The Harvard Brain Spring 2020 by theharvardbrain

THE HARVARD BRAIN SPRI NG 2020 MASTHEAD Edit or -in-Chief Amanda Yang '22

Wr it ing Edit or s Andrew Ham '22

Sponsor s The Harvard Brain would like to thank the Harvard Society for Mind, Brain, and Behavior for its support of our publication.

Isabella Trasolini '23 Bhargavi Garimella '23 Christine Lee '23

Layout Edit or s

Acknowledgm ent s Thank you to Shawn Harriman for his support of The Harvard Brain and Jonathan Yuan for designing the front cover of this issue.

Bhargavi Garimella '23 Christine Lee '23

Graphics Edit or William Drew '21

Out r each Chair

Not e The statements and views presented in The Harvard Brain are solely those of the authors. They do not represent and are not endorsed by The Harvard Brain or any of its sponsors and affiliates.

Andrew Ham '22

LETTER FROM THE EDI TOR-I N-CHI EF Dear Reader s, Welcom e to The Harvard Brain, Har var d?s only under gr aduate jour nal dedicated to the study of m ind, br ain, and behavior (M BB)! This is the fir st issue of the r eboot of The Harvard Brain, and I cannot be m or e excited to shar e it w ith you all. W ith this r eboot, The Harvard Brain takes a new for m , and, as you w ill soon see, this inaugur al issue featur es a br oad r ange of content, including scientific ar ticles, com m entar ies, under gr aduate r esear ch w or k, book r eview s, and inter view s w ith pr om inent M BB-r elated pr ofessor s. One of the goals of The Harvard Brain is to pr om ote an inter disciplinar y appr oach to fur ther ing our under standing of hum an behavior and m ental life. In line w ith this m ission, The Harvard Brain ser ves as a platfor m for under gr aduates to exam ine M BB-r elated topics fr om a w ide r ange of per spectives, including (but not lim ited to) the seven fields par ticipating in the Har var d M BB Inter faculty Initiative: psychology, neur oscience, philosophy, linguistics, hum an evolutionar y biology, histor y and science, and com puter science. Another goal of The Harvard Brain is to not only str engthen and help foster the M BB dialogue at Har var d College, but also help expand this im por tant inter disciplinar y dialogue nationally am ongst under gr aduates. Indeed, this issue pr oudly show cases the insightful w or k of m any Har var d College students as w ell as under gr aduate students at other univer sities acr oss the countr y. I hope that you enjoy r eading the stellar pieces in this inaugur al issue. M or eover , I hope the topics featur ed her e deepen your inter est in the hum an quest of under standing the m ultidim ensional natur e of the hum an m ind, br ain, and behavior. Happy r eading, Am anda Yang Editor -in-Chief The Harvard Brain

TABLE OF CONTENTS Com m ent ar ies Treating Opioid Use Disorders During and Post-COVID-19 | Kar ina Ascunce | 43-44 Persuasion and Climate Change (And Why Older People May Dismiss Greta Thunberg)| Anika Brahm bhat t | 45-46 The Limbic System in Lockdown: Why are we all dying our hair in quarantine? | Let izia Ye | 47-48 Attention Deficit Hypermobility Disorder? Connecting the dots between the body and the brain | S. Jade Bar clay | 49-51

Or iginal Resear ch Inside the Brains of Man?s Best Friend: An Study of Evolutionary Neurobiology | Kelsey Hoskin | 52-53 Understanding Two Year Old Children?s Poor Performance on a Task of Selective Sustained Attention: Perseveration and Spatial Resolution Errors on the TrackIt Task | Megan Maxwell | 54 Magical Thinking and its Role in Contemporary Fantasy Media | Jonah Goldberg | 55-56 Neural Indicators of Social and Emotion Regulation | Grace Ander son | 57-58 Moral Foundations in the Coronavirus Pandemic | Riley Hof f m an | 59-60

Pr of essor I nt er views ?Everything Was Interesting?: Exploring the Minds of the Carey Lab | Audr ey Jones | 61-63 Implications of COVID-19 and technology on education: An Interview with Cognitive Psychologist Daniel Willingham | Ser ena Chm elar | 64-66

TABLE OF CONTENTS Book Reviews Descartes?Error | At hena Capo-Bat t aglia | 67

Shor t St or y Spirited Away | Just in Wong | 68-69

Soci al l y Pr escr i bed Per f ect i on i sm an d I t s N egat i v e Con t r i bu t i on s t o Col l ege St u d en t s?M en t al H eal t h H uong Le H ar var d College '22 M ajor : N eur oscience

Since 9th grade, Aubrey has always been a perfect student. Her goal was to get an A in everything and be well-rounded. Nevertheless, things changed when Aubrey started college. The challenging academic environment combined with peer pressure made her become more stressed and pressurized to work harder. Despite putting so much effort into studying, Aubrey got her first B in college. She vowed not to hang out with friends, have regular meals in the dining hall, or engage in any campus events until she was done with finals. Soon, Aubrey was consistently sacrificing her health to maintain her perfection (Pascucci, 2004). In today?s competitive college environment, Aubrey is a typical example of a college student affected by perfectionism. So, what is perfectionism and its relation to American college students? I. I nt r oduct ion: What is per f ect ionism ? Perfectionism broadly refers to one?s tendency to set unrealistically high personal standards and critically evaluate oneself. Hewitt and Flett (1991) conceptualized perfectionism as a multidimensional personality trait with three categories: self-oriented perfectionism (when one sets their own standards and criticizes their behaviors based on said standards), other-oriented perfectionism (when an individual imposes unrealistically high expectations on other people), and socially prescribed perfectionism, or SPP (when a person bases their behaviors on people?s expectations to gain social approval). This article will focus on the effects of SPP on college students?mental health, as this dimension of perfectionism has been found to positively correlate with many mental health problems common among students (Curran & Hill, 2017).

II. Fact or s causing t he incr easing pr evalence of per f ect ionism am ong college st udent s The prevalence of perfectionism among college students is increasing; research studies conducted by Curran and Hill (2017) revealed that, from 1989 to 2016, an average college student ?s score for SPP increased by as much as 32%. This shows that recent generations of college students are setting higher personal and academic expectations for themselves than previous generations (Curran & Hill, 2017). One reason for this increasing prevalence of perfectionism is that the United States has become more individualistic (Smith et al, 2018). This increase in individualist culture in the U.S. is promoted by changes in socioeconomic structure, secularism, and modernization (Hamamura, 2011). This change in culture places an emphasis on independence, self-development and achievement, which pressures individuals to over-exert themselves. Moreover, an influx of immigrants has also contributed to this increasing prevalence of perfectionism in the United States. The children of immigrants do not want to disappoint their parents and have their sacrifices go to waste. As a result, they work harder in schools to be ?perfect ? and successful to make their parents proud (Curran & Hill, 2017). These cultural factors encourage students to strive for increased perfection in their academic and extracurricular performance in school. III. Why per f ect ionism is a pr oblem am ong college st udent s Studies have shown that SPP has a strong association with many mental health problems among the college population (Curran & Hill, 2017). As cited in Smith?s et al. reviews, SPP leads to an increase in depressive symptoms

more than other dimensions of perfectionism (2018). The combination of perfectionism and the competitive college environment leads to an amplification of the negative effects that perfectionists experience. College perfectionists, for example, suffer from more intense periods of depressive symptoms, which in extreme cases can lead to suicidal thoughts (Flett, Hewitt, & Weber, 2014). This paper will discuss the relationships between perfectionism and depression, as well as outline possible solutions. III.

Depr ession and per f ect ionism

The pr evalence of depr ession am ongst college st udent s & why it m at t er s Depression is the most common mental health problem among university students in the United States of America (Ibrahim, Kelly, Adams & Glazebrook, 2013). According to the American Psychiatric Association (2013), depression is a state of mind when one lacks motivation, experiences feelings of worthlessness, and undergoes anxiety and poor concentration. These symptoms impair students? interpersonal, academic, and psychological functioning, contributing to their negative outlook on life (Smith et al., 2018). While an average 30.6% of undergraduates experience symptoms of depression (Smith et al., 2018), the percentage of students suffering from depression can escalate up to 84% (Ibrahim et al., 2013). Moreover, incidents of depressive symptoms among undergraduates are threefold higher than the general population. This increase in prevalence of depression is significant, as it affects students?ability to perform well in schools and excel in their extracurricular activities. How socially pr escr ibed per f ect ionism incr eases t he r isk and sever it y of depr ession am ong college st udent s Research cited by Curran and Hill (2017) has found a strong link between SPP and depression. These society-influenced perfectionists experience the most debilitating effects of depression, as they take people?s expectations of them more seriously than self-oriented and other-oriented perfectionists (Curran & Hill, 2017). This is because the expectations that society imposes upon students are often overwhelming: they are expected to achieve a certain grade point average, maintain their strong academic performance, and choose a good major that will lead to a sustainable career post-graduation (Hewitt & Flett, 1991). Therefore, students force themselves to try harder to meet such standards, and when they cannot keep up with the pressures, the resultant failures make them feel worthless, rejected, and unwanted by others (Smith et. al, 2013).

These emotional effects gradually increase their depressive symptoms and may lead students to isolate themselves from their community. Since SPP is maladaptive, it prevents students from reflecting on and learning from their failures, so they instead fixate on temporary shortcomings. With this cycle, ongoing disapproval and shortcomings further lead to social hopelessness (Smith et al., 2013). Many students will feel that nothing can be changed from current situations and will likely be more depressed. Existing research demonstrates that college students who consider themselves as perfectionists reported more frequent depressive episodes and lower self-esteem scores than those who rated themselves as non-perfectionists (Smith et al., 2013). This difference in the frequency of depression between perfectionists and non-perfectionists supports the notion that perfectionism increases this mental health problem among college students. I V. Pr oposed solut ions Despite the increasing prevalence of depression due in part to higher levels of perfectionism among college students, insufficient efforts have been made to alleviate this mental health problem and discourage the need for perfectionism. According to Eisenberg and Chung?s research study regarding the adequacy of depression treatment in U.S. college students, fewer than half of depressed students received any type of mental health treatment (2012). Among students suffering serious depressive symptoms, only 22% received antidepressants or counseling at a minimally adequate level (Eisenberg & Chung, 2012). These data suggest that counseling and health support services in colleges and universities have failed to provide effective assistance Figur e 1: Perfectionism and its to their students, as relationships with depression.

they neglect a great number of those experiencing the effects of depression. One way to solve this problem might be to focus more on building stronger counseling services on college campuses. Instead of having students reach out to the mental health services, the counselors should attempt to contact students first to build a trusting relationship with them. Then, through monthly check-up appointments, they can constantly monitor students?behaviors and mental state to intervene on time if students show signs of depression or suicidal thoughts. Multiple research studies cited by Downs, Alderman, Schneiber, & Swerdlow (2016) indicate that early interventions and constant follow-ups from schools?mental health services can reduce depression in students. Another way that colleges could alleviate mental health problems is building a more collaborative community that encourages students to share their concerns and stress with others. This can be done through anonymous peer-to-peer counseling. Since students are surrounded by friends and are more likely to turn to them for help when struggling with mental health problems, this approach provides an inexpensive and largely available resource for students beyond the traditional mental health services (Kirsch et al., 2014). Moreover, these support networks have been found to reduce the stigma associated with help-seeking and improve student ?s mental health conditions (Kirsch et al., 2014). Peer counseling?s stigma-reduction aspect can benefit college perfectionists who experience depression. These students have demonstrated better interactions with people around them; they also view society less negatively and show higher levels of hopefulness and empowerment (Lloyd-Evans et al., 2014). Another solution that colleges can use is promoting mindfulness among undergraduates. According to Chesin and Jeglic (2016), mindfulness refers to one?s ability to view their actions with an accepting and reflective attitude. Instead of creating further self-criticism and mistake fixation within individuals, mindful thinking promotes the opposite effects. It allows them to be more lenient on themselves for making mistakes and value their personal growth more than over the perfect grades or recognition they receive from society and peers. Colleges should incorporate mindfulness programs? such as regular yoga and meditation sessions? that allow students to step back, challenge their thoughts, and reflect on the attainability of their goals. This can reduce students? tendency toward perfectionism and depression (Chesin & Jeglic, 2016).

Conclusion: Over the past 30 years, an increasingly individualistic culture in the United States has given rise to a more perfectionistic student population, one which lives constantly under the impression of having to keep up with societal expectations. The fact that SPP makes students more susceptible to mental health problems suggests that perfectionism plays an important role in shaping students? overall health. While perfectionism is a trait adopted by students, colleges and universities should play an active role in helping these young people utilize their potential, set realistic goals, and maintain a growth mindset. By aiming to reduce perfectionism, schools will not only improve students?health and academic performances but also build a more collaborative community where students are free to express their thoughts and concerns. All in all, more research focusing on methods to reduce perfectionism is essential for the protection of college students? mental health as they enter one of the most stressful periods of their lives. Ref er ences Chang, E. (1998). Cultural Differences, Perfectionism, and Suicidal Risk in a College Population: Does Social Problem Solving Still Matter? Cognitive Therapy and Research, 22(3), 237-254. Chesin, M., & Jeglic, E. (2015). Factors Associated with Recurrent Suicidal Ideation among Racially and Ethnically Diverse College Students with a History of Suicide Attempt: The Role of Mindfulness. Archives of Suicide Research, 20(1), 29-44. Curran, T., & Hill, A. (2017). Perfectionism Is Increasing Over Time: A Meta-Analysis of Birth Cohort Differences From 1989 to 2016. Psychological Bulletin. No Pagination Specified. http://dx.doi.org/10.1037/bul0000138 Downs, N., Alderman, T., Schneiber, K., & Swerdlow, N. (2016). Treat and Teach Our Students Well: College Mental Health and Collaborative Campus Communities. Psychiatric Services, 67(9), 957-963. Eisenberg, D., & Chung, H. (2012). Adequacy of depression treatment among college students in the United States. General Hospital Psychiatry, 34(3), 213-220. Flett, G., Hewitt, P., Heisel, M., & Alexander, M. (2014). The Destructiveness of Perfectionism Revisited: Implications for the Assessment of Suicide Risk and the Prevention of Suicide. Review of General Psychology, 18(3), 156-172. Hamamura, T. (2012). Are Cultures Becoming Individualistic? A Cross-Temporal Comparison of Individualism-Collectivism in the United States and Japan. Personality And Social Psychology Review? 16(1)?3-24. Hewitt, P., & Flett, G. (1991). Perfectionism in the Self and Social Contexts: Conceptualization, Assessment, and Association With Psychopathology. Journal of Personality and Social Psychology, 60(3), 456-470. Hewitt? P.? Flett? G.? & Weber? C. (1994). Dimensions of perfectionism and suicide ideation. Cognitive Therapy and Research?18?439-460. Ibrahim, A., Kelly, S., Adams, C., & Glazebrook, C. (2012). A systematic review of studies of depression prevalence in university students. Journal of Psychiatric Research, 47(3), 391-400. Illinois Department of Public Health. (n.d.). Suicide and College Students. Retrieved December 10, 2018, from http://dph.illinois.gov/topics-services/prevention-wellness/suicide-prevention#publications-publications-suicide Kisch, J., Leino, E. V., & Silverman, M. M. (2005). Aspects of suicidal behavior, depression, and treatment in college students: Results from the Spring 2000 National College Health Assessment Survey. Suicide and Life-Threatening Behavior, 35(1), 3-13. Kirsch, D., Pinder-Amaker, J., Morse, S., Ellison, L., Doerfler, C., & Riba, M. (2014). Population-Based Initiatives in College Mental Health: Students Helping Students to Overcome Obstacles. Current Psychiatry Reports,16(12), 1-8. Lloyd-Evans, B., Mayo-Wilson, E., Harrison, B., Istead, H., Brown, E., Pilling, S., . . . Kendall, T. (2014). A systematic review and meta-analysis of randomized controlled trials of peer support for people with severe mental illness. Bmc Psychiatry, 14(1), 39. Mackenzie, S., Wiegel, J., Mundt, M., Brown, D., Saewyc, E., Heiligenstein, E., Harahan, B., & Fleming, M. (2011). Depression and Suicide Ideation Among Students Accessing Campus Health Care. American Journal of Orthopsychiatry, 81(1), 101-107. Pascucci, M. (2004, n.d). In Pursuit of Perfection: Students Who Are Overachievers May Pay a High Psychological Price. Campus Calm. Retrieved December 5, 2018. http://www.campuscalm.com/college-perfectionism.html Smith, M., Sherry, S., Mclarnon, M., Flett, G., Hewitt, P., Saklofske, D., & Etherson, M. (2018). Why does socially prescribed perfectionism place people at risk for depression? A five-month, two-wave longitudinal study of the Perfectionism Social Disconnection Model. Personality and Individual Differences, 134, 49-54. Harvard Yard, Harvard University by Daderot / GFDL https://upload.wikimedia.org/wikipedia/commons/2/2c/Harvard_Yard%2C_Harvard_University.JPG

Th e N eu r osci en ce of M or al i t y

Var sha Swam y Univer sity of Califor nia, Los Angeles '20 M ajor : N eur oscience, M inor : Philosophy

Imagine this: You are taking a relaxing stroll near railway tracks when you notice five people in a row tied to the tracks. Suddenly, you hear a noise and look up to see a runaway trolley hurtling toward them. There is a lever right next to you that can divert the trolley to a side track. If you pull it, you can save the five people. But there is a consequence: the side track has one person tied to it. Would you pull the lever to save the five despite the one death that would occur instead? Most people say yes (Cushman, Young, &amp; Hauser, 2006). After all, one dead is better than five dead. Now, what happens if we change up the situation a bit? This time, you are on a footbridge overlooking that same track with the runaway trolley. And this time, there is no lever to pull to save the five people tied down. However, there is someone on the bridge with you - a large, heavy man. If you quickly push him off so that he falls into the path of the trolley, it will stop due to his hefty mass and the five people on the track will survive. Of course, the man you push off the bridge will die in the process. Would you do it? Would you grab this random stranger, ignore his screams of protest, wrestle him to the edge, and with one final shove, end his life so that the trolley does not hit the five people in its path? This time, most people say no (Cushman, Young, &amp; Hauser, 2006). This is interesting considering that it yields the same result as before: one dead versus five dead. The key difference between the cases lies in whether the dilemma is ?personal? or ?impersonal.? Personal moral dilemmas involve direct action, like pushing the man off the bridge. Impersonal moral dilemmas involve only indirect action, like pulling the lever to divert the train.

Emotion is one of several aspects influencing our moral judgment, especially in personal moral dilemmas. This intuitive relationship has been evidenced by neuroimaging studies. They have shown that brain areas involved in emotion processing are activated while the participant performs tasks involving moral judgment (Greene et al., 2001). While neuroimaging studies indicate a link between emotion and moral judgment, they are unable to determine whether these areas of the brain are necessary for normal moral decision-making. Dr. Michael Koenigs and his team decided to tackle this question by investigating moral decisions of patients with damage in one such brain area. This brain structure, the ventromedial prefrontal cortex (vmPFC), projects to brainstem and basal forebrain areas that are integral for emotional response (Ongur, 2000). Patients with vmPFC damage have diminished social emotions, including shame and compassion. The adultonset vmPFC damage patients chosen by Dr. Koenigs, while deficient in emotional response, retained strong logical reasoning skills and declarative knowledge of moral norms. The study also involved neurologically normal subjects as a control. Using the trolley examples, we can see that there are two competing considerations that result in the final decision. The first is a utilitarian approach, which strictly evaluates benefits versus costs. For example, someone using the utilitarian approach would push the man off the bridge, strictly due to the comparison of one versus five lives lost. The second consideration is emotional aversion. Most people have a strong emotional aversion to an action that would directly hurt someone, like pushing the man off the bridge.

If the effect of the vmPFC on emotions is necessary for normal moral decision-making, then in personal moral dilemmas, the vmPFC-lesioned subjects would show a higher rate of 3 utilitarian responses than the control. The results of Dr. Koenigs? experiment supported this prediction. During impersonal moral dilemmas based on indirect action, vmPFC subjects and control subjects had a similar rate of utilitarian decisions (Koenigs et al., 2007). During personal moral dilemmas based on direct action, vmPFC subjects had nearly double the rate of utilitarian decisions compared to control subjects. This implies that the vmPFC?s effect on emotional processing is indeed essential for normal moral judgment, specifically in cases of direct action.

Ref er ences Cushman, F., Young, L., &amp;amp; Hauser, M. (2006). The Role of Conscious Reasoning and Intuition in Moral Judgment. Psychological Science, 17(12), 1082-1089. doi:10.1111/j.14679280.2006.01834.x Greene, J. D. (2001). An fMRI Investigation of Emotional Engagement in Moral Judgment. Science, 293(5537), 2105?2108. doi: 10.1126/science.1062872 Koenigs, M., Young, L., Adolphs, R., Tranel, D., Cushman, F., Hauser, M., &amp; Damasio, A. (2007). Damage to the prefrontal cortex increases utilitarian moral judgements. Nature, 446(7138), 908?911. doi: 10.1038/nature05631 Ongur, D. (2000). The Organization of Networks within the Orbital and Medial Prefrontal Cortex of Rats, Monkeys and Humans. Cerebral Cortex, 10(3), 206-219. doi:10.1093/cercor/10.3.206 Taber-Thomas, B. C., Asp, E. W., Koenigs, M., Sutterer, M., Anderson, S. W., &amp; Tranel, D. (2014). Arrested development: early prefrontal lesions impair the maturation of moral judgement. Brain, 137(4), 1254?1261. doi: 10.1093/brain/awt377 Trolley problem by McGeddon / CC BY-SA 4.0 https://upload.wikimedia.org/wikipedia/commons/8/8c/Trolley_problem.png

A key aspect of moral judgment not discussed thus far is the idea of self-interest. To illustrate this, let ?s say you are on a lifeboat with two others, but the weight is over the boat ?s capacity. Your weight is double that of each of the other passengers, such that in order for the boat to stay afloat, either you have to go or both of them do. Would you push the other two off, or jump off yourself? The self-serving decision would be to push the other two off. Over the years, researchers delved into this topic of self-interest in moral judgment while studying the vmPFC. Dr. Bradley Taber-Thomas and his team researched the moral judgment of individuals with developmental vmPFC damage. The other groups involved in the study were adult-onset vmPFC damage patients and neurologically normal control subjects. Results showed that the developmental vmPFC damage patients exhibited self-serving behavior in low-conflict self-serving situations over twice as often as both other groups (Taber-Thomas et al., 2014). This implies that the vmPFC is essential for learning social and moral norms. Interestingly, it is likely not essential for using those norms once learned, since the adult-onset patients did not show excessive self-serving behavior. As someone studying both neuroscience and philosophy, I am personally fascinated by this overlap between moral judgment and neuroscience. Studies like the two mentioned here 4 have crucial implications for various disciplines, including law. Imagine that a perpetrator has neurological vmPFC damage and that the unlawful actions he committed involved a direct action moral judgment. Does this mean that there are grounds for the perpetrator to be acquitted of his crime? This question, and many others that arise, are important to think about as new developments come to light in this exciting field.

Gaby 's Road t o Recov er y Sam antha H er r er a H ar var d College '23 M ajor : N eur oscience Gaby Flores is a devout Christian. While living in Mexico, she attended church every Sunday, and she was well-known by the church staff. So, when in 2013, she was absent, the church staff was concerned. They attempted to get in touch with one of her sons since she sometimes went to spend the weekend with him. He told them that she was at her home. This troubled the pastor, who decided to check on her. The pastor went to her house, but there was no sign of Gaby. He looked through a side window and saw a woman on the floor. He used an emergency spare key to enter the house and check on her. She was in a very bad state. It would later be discovered that she had fallen and had lain on the floor for three days before being found. At the hospital, they found Gaby had hit her head and had a brain bleed. She was rushed into surgery to remove the accumulated blood and implant a valve to continue to drain any blood. Despite these measures, her condition didn?t improve. They eventually found that they had implanted the wrong kind of valve and blood was still gathering in her head. They changed the valve and continued to monitor her condition. Gaby was conscious but extremely confused. Due to the long time that it took them to find the problem, her brain had been extremely damaged ? the doctors were convinced it was permanent. Her family wanted to bring her to the United States, where most of her family lived, for a second opinion, but the doctors thought she was too delicate to travel. Two months later, her situation was bad, but had plateaued. Doctors

cleared her for travel, but warned she would most likely die soon. Her family brought her to the US. Gaby was admitted into the hospital after only a couple hours on American soil. Her family was waiting in an outside waiting area to see her. I was one of those family members; . Gaby is my great-grandmother. I loved her a lot, but I knew her mostly through family stories. Sitting outside the hospital, surrounded by family trying to be optimistic, I was hoping it wasn?t too late to get to know her better. We went in in small groups to see my great-grandma. She was conscious, but barely, and was in deep confusion the whole time, barely keeping her eyes open. She didn?t know where she was or who these people were that were in her room, but she seemed to understand that she was safe. Gaby underwent surgery the next morning, and this time, we saw immediate results. She became conscious of where she was and with who, and she started remembering events and names. After a month, she was allowed to go home. Gaby went to live with one of her daughters, Silvia, and continued to get better. Her mind became focused again and she began to move and walk. She had regular checkups with her neurosurgeon and was improving greatly. Four years later, in 2017, it was like the fall never happened. Despite being 87 years old, Gaby was strong, with a sharp mind and quick wit. Her favorite activity was walking in the park and feeding

the ducks. It was on one such walk where things changed. She was walking with some family and got tired. She took a seat on the walker that they had brought for her, and she was being pushed along when a walker wheel got caught in a crack. She fell and hit her head on the concrete. Everyone was worried, but she was walking and talking normally. She never lost consciousness or got disoriented. The family disagreed on whether to take her to the hospital. Gaby argued that she was perfectly healthy and did not need a doctor. Gaby?s legal caretaker agreed. Gaby was not taken to the hospital. The next morning, my great-aunt checked on Gaby. She found her completely rigid and unresponsive. She was taken to the hospital. They found she had a brain bleed and a clot. My great-grandma was rushed into surgery. The surgery went well, but she wasn?t much better. She was on a ventilator for fourteen days. The doctors thought she would need it longer, but they didn?t want to affect her lungs. She had a feeding tube, breathing tube, and another valve to drain blood. She experienced convulsions, which nobody could explain. After two weeks, the doctors notified us that she was going to need a second surgery to improve her status.

Gaby?s doctors in Mexico didn?t do right by her. They made an error which could have caused irreversible brain damage. They gave up on her. They did not see her improving, and instead of coming up with another solution, they signed her off as a lost cause. It wasn?t until my great-grandmother was seen by the neurosurgeon at the California hospital that we found someone willing to try. It gave us hope that someone was willing to fight for my great-grandmother as much as we were. She?s here today ? walking, talking, breathing, eating, laughing, living ? thanks to the ingenuity and determination of a neurosurgeon who took a chance on a woman who had been written off as dead.

There were post-operation complications. It took her a long time to recover from anesthesia. Her valve was constantly draining blood, as her brain was steadily bleeding. One month later, the bleeding had stopped, and she was placed in a convalescent home. She was there for nearly three years. When she returned home with Silvia, she could breathe and eat normally. Today, Gaby is 90 years old. Her mind is very good, despite her age and accidents. She loves to talk to visitors. She tells marvelous stories about the family and her life, interjected with jokes. She loves being with family, even though she misses Mexico. She uses a wheelchair, but has now begun to walk.

For get M e N ot : Th e N eu r osci en ce of Act i v e For get t i n g M ech an i sm s Jacob H er shenhouse Univer sity of Califor nia, Los Angeles '22 M ajor : N eur oscience In t r odu ct ion

Back gr ou n d

Long considered a shortcoming, the ability for animals to forget plays a pivotal role in the properly functioning brain. Intuitively, it is reasonable to assume that humans forget memories passively, as the body ages and cells degrade, but several pioneering research studies this decade have led to remarkable insights on the active neural mechanisms that result in a memory being forgotten. It is now known that the forgetting process is constantly underway in the brain and requires the recruitment of various cells, proteins, and enzymes to work efficiently. Neuroscientists have identified numerous ways through which we delete, blur, or erode memories and each plays a role in how we forget. While the memory research being conducted today is still relatively nascent, it is leaps and bounds beyond what could be undertaken with scientific equipment a decade prior (Davis & Zhong 2017). This new research enables us to better understand how forgetting facilitates our ability to extrapolate under novel circumstances. The goal of this article is to summarize the brilliant research of several neuroscientists so that their work can be understood and enjoyed by a broader audience.

Autobiographical episodic memory? memory of those events which are experienced firsthand? is activated when a present circumstance reminds you of your past. The storage of autobiographical memories is complex and activates several parts of the brain. This process involves the recruitment of millions of players to form even a single memory and it is undertaken on the cellular level. Neurons communicate with each other using chemical signals. Each neuron releases several small signaling molecules into the miniscule junction between them called the synapse. Each neuron has synaptic connections with thousands of other neurons and possesses intermembral receptors to receive the chemical signals from their neighbors. Neurons are constantly remodeling their synapses to selectively control the strength of the signals they receive (Davis & Zhong 2017). A specific network of cells within the larger web is activated when a particular memory is recalled. The more it is recalled, the stronger the connection becomes such that the memory is more easily recalled (Gravitz 2019). There still remains much unknown information regarding how memories are created, stored, and recalled, but this foundational understanding has given scientists a framework in which to further their research on the inner workings of the mind. ?Every species that has a memory forgets,? says Michael Anderson, a

cognitive neuroscientist at the University of Cambridge, ?It doesn?t matter how simple the organism is: if they can acquire lessons of experience, the lessons can be lost? (Hulbert & Anderson 2018). Yet, why is this the case, and how is it beneficial? Ron Davis an d Drosophila melanogaster Ron Davis is a neuroscientist at the Scripps Research Institute in Florida. In 2012, Davis and his research team were studying memory formation in fruit flies. Fruit flies are an especially good research specimen because they are easy to breed and have approximately 100,000 neurons compared to man?s 100 billion neurons (Zheng et al. 2018). Looking specifically at dense areas of neurons, termed mushroom bodies for their shape, which store sensory data for the fly, Davis? team found an incredible link between memory and the neurotransmitter dopamine (Berry, Davis et al. 2012). Dopamine is essential to a number of neural processes, including those that result in feelings of happiness and reward. To test its correlation to memory, Davis? team devised an experiment in which the team trained flies (through classical conditioning) to associate certain scents with the delivery of an electric shock. Once the association was made, they postulated that when they increased the dopamine levels in the neurons of the mushroom body and reintroduced the fly to the scented environment, the flies would have a heightened awareness of the smell. Yet, when the activation of neurons that moderate dopamine levels was undertaken, they observed that the fruit flies had forgotten the association. Inversely, when

blocking these same dopamine secreting neurons, the negative memory of the scent was preserved (Berry, Davis et al. 2012). This experiment provided concrete evidence that dopamine was a major factor in the elimination of episodic memory and moreover proved that forgetting cannot be separated from other functions dopamine serves in the brain. Davis had then found that the brain does not only erode memories over time due to cell damage and other factors, rather it actively works to forget what we do not need. This led Davis to publish his paper on the multiple roles that dopamine plays in learning and forgetting, indicating a need for more research to be conducted on the subject to elucidate the human impact of these findings. Oliver Har dt an d r at s r u n n in g m azes Oliver Hardt, a psychologist at Montreal?s McGill University, built upon Davis?work with his research on slightly larger test subjects? rats. Hardt focused his study on the area of the brain known as the cortex, where long term memory is housed, and his lab challenged a fundamental problem of complexity in what they observed. They were studying AMPA receptors, which mediate fast synaptic transmission throughout the central nervous system and brain (Chater & Goda 2014). This means AMPA receptors are present at the synapses of neurons and are essential to maintaining the function of the cells which transmit long term memories. The problem was that AMPA receptors were being removed and created anew over the course of days or even hours (Migues, Hardt et al. 2016). Their breakthrough came when they were able to block the biochemical mechanism

that led to the removal of AMPA receptors at the synapse. In their experiment, they employed the interference peptides GluA23Y and G2CT (proteins that affect glutamate levels) to inhibit the AMPA receptor removal mechanism in their rats. What they found was blocking the turnover of AMPA receptors prevented the natural forgetting of long-term memories. Inhibited rats were statistically more able to remember the maze they had run each day than normal rats who served as the control group (Migues, Hardt et al. 2016). Essentially, blocking the removal of these AMPA receptors meant that memories were retained for a longer period of time. This demonstrated that the synaptic removal of AMPA receptors was another key player in the active forgetting process and further detailed that forgetting is biologically intentional, not only a product of erosion over time. Pau l Fr an k lan d an d n eu r ogen esis Hundreds of miles from Hardt, at the University of Toronto?s Hospital for Sick Children Research Institute, a scientist named Paul Frankland was attacking the issue from a different angle. Frankland found that the creation of new neurons, a process known as neurogenesis, catalyzes the loss of memory in experiments run with guinea pigs and adult mice (Akers, Frankland et al. 2014). Neurogenesis is the cellular process by which the brain grows in childhood and adolescence. It was long believed that neurogenesis was inactive in the adult brain; however, recent research has shown that neurogenesis continues in the dentate gyrus, an area of the hippocampi of mature animals (Cameron and Glover 2015). The goal of Frankland?s research was to determine whether neurogenesis in

mature mice improved their memory function. They discovered contradictory evidence to what they had initially hypothesized; they amazingly learned that the creation of more neurons in mature mice decreases the capacity to retain memory (Akers, Frankland et al. 2014). Though this is seemingly counterintuitive, Frankland rationalized the data by interpreting the creation of new neurons as a disruption of the existing network of neurons that store memory. They came to understand that introducing new neural cells through mature neurogenesis was essentially like forcing more pieces into an already complete puzzle. This realization also helps explain why the long-term memory of infants, who are experiencing prolonged and rapid neurogenesis, is so fruitless. Wh y f or get t in g is essen t ial (an d f r u st r at in g) f or h u m an s This research above has made significant contributions to this area of scientific study and allows us to begin to draw conclusions about the importance of these different players in the human brain. The biggest question is what is the functional and evolutionary purpose of our brains actively making us forget? Put simply, forgetting allows animals to adapt to a changing environment. Sometimes when one is tasked with a semantic recall activity such as reciting the first one hundred digits of pi or remembering the minor characters of a novel from childhood, one wishes that they had a perfect, limitless memory in which they remember every detail of each day to a tee. For some individuals, those with highly superior autobiographical memory (HSAM), this is reality. They are able to remember on any given day what the weather was like, what they wore, or what they

ate for dinner. But despite this incredible autobiographical recall, many with HSAM see their heightened memory as a curse rather than a blessing. These individuals say HSAM hinders daily life and tends to challenge their careers and relationships due to an increased tendency for obsessiveness (Mazzoni et al. 2019). Individuals living with HSAM demonstrate, in this way, a dampened ability to apply old knowledge to novel experiences. In evolutionary terms, environmental adaptation becomes a challenge, and increased memory retention could hinder one?s biological fitness. Our environment is ever changing, and animals are required to adapt to new situations to survive. As biologist and computer scientist Blake Richards posits, ?our ability to generalize new experience is, at least in part, due to the fact that our brains engage in controlled forgetting? (Gravitz 2019). In this way, memory and forgetting are baked into our evolution and give us the capability to make sense of our world. Con clu sion Recent discoveries have made the neural process of active forgetting a hot topic in neuroscientific research. The work of trailblazing scientists such as Davis, Hardt, and Frankland, is inspiring and draws a more detailed picture of our brain on the microscopic scale. Perhaps contrary to popular belief, forgetting is not an accident. These scientists provided evidence to show how our brain actively tries to forget, why it is important that we do so, and how different biochemical players affect the process of forgetting. Dopamine, AMPA receptors, and neurogenesis are all involved in the active process of forgetting and are all important to other essential functions of the brain, so we must accept that

forgetting is an evolutionarily integral part of life.

conserved

and

While this research sheds light on the neuroscience behind some of the process, more dedicated research is required for us to gain a more accurate grasp on how we remember and forget. Yet, with advanced technology and a global network of researchers, the near future of neuroscience is more promising than ever. Ref er en ces Akers KG, Martinez-Canabal A, Restivo L, Yiu AP, De Cristofaro A, Hsiang HL, Wheeler AL, Guskjolen A, Niibori Y, Shoji H, Ohira K, Richards BA, Miyakawa T, Josselyn SA, Frankland PW (2015). Hippocampal neurogenesis regulates forgetting during adulthood and infancy. Science, 344(6184):598-602. https://doi.org/10.1126/science.1248903 Berry, JA, Cervantes-Sandoval, I, Nicholas, EP, & Davis, RL (2012). Dopamine is required for learning and forgetting in Drosophila. Neuron, 74(3), 530?542. https://doi.org/10.1016/j.neuron.2012.04.007 Cameron, H. A., & Glover, L. R. (2015). Adult neurogenesis: beyond learning and memory. Annual review of psychology, 66, 53?81. https://doi.org/10.1146/annurev-psych-010814-015006 Chater TE and Goda Y (2014) The role of AMPA receptors in postsynaptic mechanisms of synaptic plasticity. Front. Cell. Neurosci. 8:401. doi: 10.3389/fncel.2014.00401 Davis, RL, & Zhong, Y (2017). The Biology of Forgetting-A Perspective. Neuron, 95(3), 490?503. https://doi.org/10.1016/j.neuron.2017.05.039 Gravitz, L (2019). The Forgotten Part of Memory. Nature, 571:S12-S14. https://doi.org/10.1038/d41586-019-02211-5 Hulbert, JC, & Anderson, MC (2018). What doesn't kill you makes you stronger: Psychological trauma and its relationship to enhanced memory control. Journal of experimental psychology. General, 147(12), 1931?1949. https://doi.org/10.1037/xge0000461 Mazzoni G, Clark A, De Bartolo A, Guerrini C, Nahouli Z, Duzzie D, De Marcof M, McGeowng W, Vennerif A (2019) Cortex. 120:588-602. https://doi.org/10.1016/j.cortex.2019.02.020 Migues, PV, Liu, L, Archbold, GE, Einarsson, EĂ&#x2013;, Wong, J, Bonasia, K, Ko, SH, Wang, YT, & Hardt, O (2016). Blocking Synaptic Removal of GluA2-Containing AMPA Receptors Prevents the Natural Forgetting of Long-Term Memories. The Journal of neuroscience, 36(12), 3481?3494. https://doi.org/10.1523/JNEUROSCI.3333-15.2016 Zheng, Z et al. (2016) A complete electron microscopy volume of the brain of adult Drosophila melanogaster, Cell. https://doi.org/10.1016/j.cell.2018.06.019

W h en L i f e Gi v es You L em m on s: Debu n k i n g M et h aqu al on e M y t h s i n M ed i a Jillian Ubando Univer sity of Califor nia, Los Angeles '20 M ajor : N eur oscience If you were born after the 80s, chances are everything you know about methaqualone you have learned from The Wolf of Wall Street. Referring to it as ?ludes? and ?Lemmons?, the 2013 film depicted methaqualone in a comedic way that sparked many people?s interest in the drug. While the film touched upon many key aspects of the drug, such as its history, legal status, and effects, it is worth questioning how much of the information provided is dramatized and how much of it is factual. So, in the words of the on-screen Jordan Belfort, ?Don?t know what a lude is? I?ll tell you? (Winter, et al., 2013). Consistent with the film?s claim, methaqualone was indeed synthesized in 1951 by an Indian doctor looking for a cure for malaria (Brown & Goenechea, 1973). While methaqualone did not work to treat malaria, its hypnotic effects were soon discovered and various countries began looking to it as a possible sleeping aid. Early studies demonstrated methaqualone?s medical potential as a sedative, and it seemed to be a safer alternative to barbiturates (Herzberg, 2012). Both barbiturates and methaqualone bind to their specific extracellular sites on GABA-A receptors in neurons, causing increased influx of chloride ions, which hyperpolarizes the neuron and prevents it from transmitting a signal to another neuron? a mechanism responsible for feelings of relaxation

(Hammer, et al., 2015). With clinical trials from the 1960s indicating that methaqualone can have the same positive effects as barbiturates with a lower abuse potential and lower risk of overdose, this new drug seemed promising and was marketed as such. In 1965, the FDA approved the ?ethical prescribing? of methaqualone by itself under the brand Quaaludes (Herzberg, 2012). Jordan Belfort, played by none other than Leonardo DiCaprio, states that ludes were ?prescribed to stressed-out housewives with sleeping disorders? (Winter, et al., 2013), which neglects to mention just how easy it was for anyone to get their hands on ludes during its early years. Large quantities of them were prescribed, and from there, shared between friends, at large social gatherings, and even between parents and children who believed methaqualone to be safer than it actually was. So the question is, why were people so hooked on Lemmons? More importantly, why did Belfort?s comrade, the character played by Jonah Hill, look like a kid at Christmas when he revealed them on screen? It is hard to imagine why anyone would want to take Lemmons after watching DiCaprio and Hill sprawled on the floor barely able to speak. However, slurred speech and motor control impairment? among nausea, unconsciousness and vomiting? are only present at high doses, and given

that DiCaprio and Hill?s characters took not one, not two, but four tablets each, their condition surprises no one. Looking at the pill jar in the movie, they took Lemmons 714, which contained 300 mg of methaqualone per pill. For first time users, just taking 300 mg at one time was considered dangerous, especially if combined with alcohol (?Methaqualone?, 2017). In actuality, effects at the common dosage are euphoria, anxiety relief, and? oddly enough? pleasant tingling sensations. Many people did not even need to resist any urge to sleep, as sedation from Lemmons was typically mild, allowing people to take them throughout the day with no issues staying functional and coherent (Orzack, et al., 1988). Still, there is one effect in particular that The Wolf of Wall Street depicts well: disinhibition. Defined as ?impulsive actions [that] often have unwanted or even harmful outcomes? (Kristalyn, 2019), disinhibition can take different forms under various circumstances. Some people believed ludes were aphrodisiacs because they seem to increase pro-sexual behaviors, but this is now mostly attributed to disinhibition which encompasses the increase in overall risk-taking actions. This is well-demonstrated in the film as DiCaprio and Hill both almost die on Lemmons, with the former attempting to drive home motor-impaired and high, and the latter shoving exorbitant amounts of deli meats into his mouth causing him to almost choke to death (Winter, et al., 2013). As ridiculous as these scenes were, they certainly conveyed the effects of the drug to viewers. While the slurred exchanges between DiCaprio and Hill were nothing less than iconic, another apparent piece of information that the film reveals about

methaqualone is that the drug is no longer available. Between the early advertisements claiming it to be safe, and the ease by which people got their hands on it, methaqualone-use undoubtedly became widespread and problematic in America. Overdose rates spiked in the 70s as the drug proved time and time again its high addictive potential. Therefore, by 1982, the U.S. decided that the drug be put on Schedule 1, meaning that it has no acceptable therapeutic use and cannot be prescribed. Nowadays, some of the only ways to acquire them now are from other countries? mostly those in Africa? or from decade-old stashes.If neither this article nor the film has put your curiosity about ludes to rest, it is worth noting that while it is still possible to find drugs stamped as Lemmon 714s, but people should be very skeptical about buying them. The makers of The Wolf of Wall Street are not the only people who can create realistic-looking Lemmon 714s, as counterfeited pills containing little or no methaqualone are much more common than authentic ones, and also much more lethal as doses vary (Drug Enforcement Administration, 2007). This is all to say one thing: when life gives you Lemmons, don?t eat them. Ref er en ces Drug Enforcement Administration (2007, Jan.) Quaalude Lemmon 714 Mimic Tablets (Containing Diazepam) ? Surprising persistence. The Drug Enforcement Administration: Office of Forensic Sciences. https://erowid.org/library/periodicals/microgram/microgram_2007-01.pdf Hammer, H., Bader, B. M., Ehnert, C., Bundgaard, C., Bunch, L., Hoestgaard-Jensen, K., ? Jensen, A. A. (2015). A Multifaceted GABAA Receptor Modulator: Functional Properties and Mechanism of Action of the Sedative-Hypnotic and Recreational Drug Methaqualone (Quaalude). Molecular Pharmacology, 88(2), 401?420. doi: 10.1124/mol.115.099291 Herzberg, David. (2012). Busted for Blockbusters: "Scrip Mills," Quaalude, and Prescribing Power in the 1970s. Prescribed, (9), 207-231. Retrieved from https://www.researchgate.net/publication/323322431 ?Methaqualone.? The Drug Classroom, 9 Aug. 2017. https://thedrugclassroom.com/video/methaqualone/#Effects Orzack, M. H., Friedman, L., Dessain, E., Bird, M., Beake, B., McEachern, J., & Cole, J. O. (1988). Comparative study of the abuse liability of alprazolam, lorazepam, diazepam, methaqualone, and placebo. International Journal of the Addictions, 23(5), 449?467. https://doi.org/10.3109/10826088809039211 Salters-Pedneault, Kristalyn. ?Disinhibition (Impulsivity) in BPD.? Very Well Mind, Gans, Steven (Editor), 18 Aug. 2019, https://www.verywellmind.com/what-is-disinhibition-425293 Winter, T., DiCaprio, L., Aziz R., McFarland, J., & Koskoff, E. T. (Producers), & Scorsese, M. (Director & Producer). (2013). Wolf of Wall Street (Motion Picture]. United States: Paramount.

Th e Sci en ce of For get t i n g Am anda For tin Boston Univer sity '20 M ajor : N eur oscience One of the most natural things we do everyday is forget. Maybe you forgot to take the chicken out of the freezer. Or maybe you forgot about that appointment you?ve rescheduled twice now. You never remember how you forget - no one ever taught you how to forget. You just do. Research in neuroscience suggests that memory systems rule how we form and store memories. But are there also systems that help us forget? You may have heard the saying ?it?s like learning to ride a bike.? Why is it that when we learn some tasks, such as riding a bike, it?s like we know the task forever? This type of skill is often referred to as a procedural memory. The motor memories that help you learn and remember how to play Fur Elise are ruled by a memory system that is distinct from what helps you remember what you did for Halloween last year. The latter type of memory is a personally experienced event, otherwise known as an episodic memory (Tulving, 1993). The former system relies heavily upon structures within the basal ganglia. These structures can facilitate movement, but can also contribute to somewhat unconscious behaviors, like being able to type without looking at the keyboard. If you switch to a new type of keyboard, you might struggle at first - but with some adjustments, you will find that you type as fast as ever (Graybiel et al., 2015). Episodic memories are thought to rely upon the functioning of the hippocampus. In extreme circumstances where the hippocampus has been damaged or removed, such as with patient H.M., one can no longer form new episodic memories. After a bicycle accident left him with a treatment-resistant seizure

disorder, Patient H.M., elected to have brain surgery to remove the hippocampus, the apparent locus for his seizures. When he woke up, at first he seemed fine. Until those around him realized that he appeared to have anterograde amnesia; he was unable to form new memories. Researchers quickly flocked to patient H.M. Before H.M.?s surgery, researchers thought that memory was diffuse, unlike our sensory systems (Squire, 2009). H.M. violated this viewpoint, and even showed us that different types of memories exist. For example, he was still able to learn procedural skills and motor tasks, he just could no longer remember that he had learned them (Squire, 2009). These results are easily replicated in rodent lesion studies of the hippocampus as well. Patient H.M., laid the groundwork for understanding how we remember. But work starting with the Ron Davis lab in 2012 at The Scripps Research Institute in Florida began to elucidate how we forget. In the past, scientists largely believed that forgetting is mostly a passive process. In a study of fruit flies (Drosophila), researchers taught flies to associate a smell paired with either positive reinforcement (food) or negative reinforcement (mild electric shocks). They then analyzed the brains of the flies to determine if they remembered or forgot the information. Their key finding was that the neurotransmitter dopamine appears to regulate not only how we remember, but also how we forget (Berry et al., 2012). The key may lie in two dopamine receptors. The Davis group proposes that the ?on? switch that allows for memory consolidation lies in the dDA1 dopamine receptor, which drives memory acquisition. The ?off ? or

forgetting switch is the DAMB receptor, which appears to trigger our ability to forget. Stimulation and inhibition of these receptors is sufficient to influence the flies to have superior memory of the smell-reinforcement associations, or to evaporate their learning (Berry et al., 2012). If these receptors exist mainly in brain regions associated with episodic learning, then this might provide one reason for why procedural memories are much more stable than episodic memories. Other groups have suggested that forgetting may be enhanced while we sleep (Izawa et al., 2019). A group of neurons in the hypothalamus, a brain region largely associated with hormonal production, begins to fire in our sleep. These same cells fire and inhibit the hippocampus. By activating or inhibiting these same cells that were responsible for inhibiting the hippocampus, the group was able to show that they could force the animals to either forget or remember, respectively. This plays an interesting spin on how we think of sleep. Often, we say that we need sleep to remember - but maybe a part of sleep?s role is helping us forget. The work by Izawat et al., 2019 may also have implications beyond answering how we forget. It may provide insight into disorders like PTSD, in which patients have altered hypothalamus structure. If a functional hypothalamus is essential to forgetting, the reason PTSD patients may be unable to ?forget? their trauma is that their hypothalamus is not functioning properly. These patients may struggle to reduce their fear to stimuli that make them recall their trauma (Herringa et al., 2012).

Dopamine receptors, the hypothalamus, and microglia all have a certain role in how we forget. However this research is just the tip of the iceberg and suggests that the brain has diverse mechanisms for making us forget. Whether these processes are connected is yet to be described. As we uncover how these processes work, we may have new insights into traditionally hard to treat psychiatric disorders and incurable neurodegenerative disorders. Ref er en ces Berry, J. A., Cervantes-Sandoval, I., Nicholas, E. P., & Davis, R. L. (2012). Dopamine is required for learning and forgetting in Drosophila. Neuron, 74(3), 530-542. Graybiel, A. M., & Grafton, S. T. (2015). The striatum: where skills and habits meet. Cold Spring Harbor perspectives in biology, 7(8), a021691. https://doi.org/10.1101/cshperspect.a021691 Herringa, R., Phillips, M., Almeida, J., Insana, S., & Germain, A. (2012). Post-traumatic stress symptoms correlate with smaller subgenual cingulate, caudate, and insula volumes in unmedicated combat veterans. Psychiatry Research: Neuroimaging, 203(2-3), 139-145. Izawa, S., Chowdhury, S., Miyazaki, T., Mukai, Y., Ono, D., Inoue, R., ... & Terao, A. (2019). REM sleep?active MCH neurons are involved in forgetting hippocampus-dependent memories. Science, 365(6459), 1308-1313) Squire L. R. (2009). The legacy of patient H.M. for neuroscience. Neuron, 61(1), 6?9. https://doi.org/10.1016/j.neuron.2008.12.023 Tulving, E. (1993). What Is Episodic Memory? Current Directions in Psychological Science, 2(3), 67-70. Retrieved from www.jstor.org/stable/20182204 Wang, C., Yue, H., Hu, Z., Shen, Y., Ma, J., Li, J., ... & Wang, L. (2020). Microglia mediate forgetting via complement-dependent synaptic elimination. Science, 367(6478), 688-694.

And yet, other researchers propose that non-neuronal units of the brain - microglia - may help us forget (Wang et al., 2020). Typically microglia are associated with ?cleaning? the brain during an inflammatory response. In this instance, microglia move through the brain, ?eating? away the molecules that support memory. This process may become pathogenic in diseases like Alzheimer ?s, where patients progressively forget older memories. Interestingly, Alzheimer ?s is marked by ?microglia culling? (Wang et al., 2020).

Fu t u r i st i c M em or y : Dev i ces t o I m p r ov e M em or y Recal l Var sha Swam y Univer sity of Califor nia, Los Angeles '20 M ajor : N eur oscience, M inor : Philosophy ?I know kung fu.? This iconic line, spoken by Neo in the classic 1999 science fiction film The Matrix, signified the successful transfer of kung fu knowledge through a direct download into his brain. The idea seemed impossibly futuristic. The question is, has the scientific community come any closer over the past few decades to achieving that potential concept of memory transfer? In the late 1990s, Dr. Sam Deadwyler and Dr. Robert Hampson began studying memory by utilizing hippocampal electrical recording and stimulation. Their team had rats perform the Delayed-Non-Match-To-Sample (DNMS) memory task while recording multi-neuron activity in the hippocampus, which is crucial for memory creation (Eichenbaum & Cohen, 2004). The DNMS task used here involves two levers: the rat must press one lever, poke its nose into a photocell located 50 cm away during a delay (variable, 1-30 seconds), then run back and press the other lever. The memory aspect comes into play during the delay, where the rat must remember which lever it has pressed already in order to press the other lever when it returns. The recordings showed that hippocampal pyramidal CA3 neurons were the most active during memory

encoding, or when the rats pressed the first lever. Pyramidal CA1 neurons were the most active during memory recall, when the rats were deciding which lever to press the second time. Dr. Hampson and Dr. Deadwyler also observed cases where the rats made the incorrect decision for the second lever press. In these error cases, the observed CA3 neuronal signal had a significantly different spatio-temporal pattern than those from accurate trials (Hampson & Deadwyler, 1996). Spatial mathematical analysis of neurons over accurate trials revealed that a specific firing pattern consistently existed for both CA3 and CA1 neurons across several rats. Dr. Ted Berger collaborated with Dr. Deadwyler ?s team in order to develop a mathematical model that could predict the spatio-temporal CA1 firing pattern based on the CA3 recording of any rat performing the DNMS task (Berger et al., 2011). Given they had already determined that CA1 firing depends on CA3 firing, Dr. Berger and Dr. Deadwyler knew that an incorrect CA3 signal would cause an incorrect CA1 signal, thus leading to an incorrect lever decision. This particular CA3 signal during error trials was considered ?weak,? as it was less spatio-temporally complete than that of an accurate trial (Berger et al., 2011). Consequently, to

make the lever decision correct following an incorrect CA3 signal, one would have to override the weak pattern with a strong pattern for the CA1 neurons at the time of lever decision. To do this, the scientists created a device that would stimulate CA1 neurons based on the CA1 pattern identified by Dr. Berger ?s model for accurate trials. This device was able to process the recorded CA3 signal, determine whether it was too weak to result in a correct lever decision and, if so, insert a corrected CA1 signal via neuronal stimulation. Note that this device does not create a false memory; rather, it uses preexisting information and simply enhances it so that poor memory can be compensated for. Without the device, the rats had an average accuracy rate of 80% for the DNMS task. With the device, that accuracy rate increased to a staggering 95% (Deadwyler et al., 2013). To further investigate the effects of the device, the scientists tested naive rats, or rats that had never completed nor been trained for the DNMS task. Naive rats had an average accuracy rate of 60%; however, with the use of the device that utilized pattern information from trained ?donor ? rats, that number jumped to slightly under 80% (Deadwyler et al., 2013). In other words, naive ?recipient? rats with the device had almost the same accuracy rate as trained rats without the device, indicating how useful the device could prove to be in real-life applications. This is an example of what memory ?transfer ? would look like. Of course, it is important to keep in mind that while rat brains and human brains both have hippocampi, they are vastly different anatomically. In order to move one step closer to the human brain, the group of scientists, collaborating with Dr. Greg Gerhardt, conducted a similar? albeit slightly more

complicated? experiment using rhesus macaque monkeys. This experiment yielded similar results, where the macaques?accuracy rate for the memory task they performed increased significantly due to the CA1 stimulation device. The stimulation patterns for this device was based on a new mathematical model specific to the observed macaque firing patterns (Hampson et al., 2014). Several other scientists have also explored the idea of memory devices. One such researcher is Dr. Michael Kahana, who recently developed an implant that stimulates the brain in order to improve memory encoding, which later improves memory recall. This was motivated by findings indicating that activity in the left lateral temporal cortex is related to successful memory encoding (Burke et al., 2014). Dr. Kahana?s device recorded activity in this area to identify weak encoding states, and then stimulated the area to return the encoding to a normal level of effectiveness. Results showed that this direct stimulation increased the probability of accurate memory recall by about 16.5% (Ezzyat et al., 2018). One important aspect of Dr. Kahana?s work is that his implant device was tested on humans rather than animals. This makes his success particularly exciting and relevant to medical device development. From Dr. Hampson and Dr. Deadwyler ?s device that acts at the time of memory recall to Dr. Kahana?s implant that corrects poor memory encoding, memory improvement remains a very interesting and exciting area at the forefront of neuroscience. Although we will not quite reach the level of science fiction seen in The Matrix anytime soon, recent strides like those discussed in this article will hopefully pave the path to successful applications

of memory enhancement in the human brain. Most importantly, these results bring us a step closer to mass production of devices that can significantly improve the daily lives of memory-impaired individuals. Ref er en ces Berger, T. W., Hampson, R. E., Song, D., Goonawardena, A., Marmarelis, V. Z., & Deadwyler, S. A. (2011). A cortical neural prosthesis for restoring and enhancing memory. Journal of Neural Engineering, 8(4), 046017. doi: 10.1088/1741-2560/8/4/046017 Burke, J. F., Long, N. M., Zaghloul, K. A., Sharan, A. D., Sperling, M. R., & Kahana, M. J. (2014). Human intracranial high-frequency activity maps episodic memory formation in space and time. NeuroImage, 85, 834?843. doi: 10.1016/j.neuroimage.2013.06.067 Deadwyler, S. A., Berger, T. W., Sweatt, A. J., Song, D., Chan, R. H. M., Opris, I., ? Hampson, R. E. (2013). Donor/recipient enhancement of memory in rat hippocampus. Frontiers in Systems Neuroscience, 7. doi: 10.3389/fnsys.2013.00120 Eichenbaum, H., & Cohen, N. J. (2004). The Hippocampal Memory System. From Conditioning to Conscious Recollection, 305-343. doi:10.1093/acprof:oso/9780195178043.003.0009 Ezzyat, Y., Wanda, P. A., Levy, D. F., Kadel, A., Aka, A., Pedisich, I., ? Kahana, M. J. (2018). Closed-loop stimulation of temporal cortex rescues functional networks and improves memory. Nature Communications, 9(1). doi: 10.1038/s41467-017-02753-0 Hampson, R. E., & Deadwyler, S. A. (1996). Ensemble codes involving hippocampal neurons are at risk during delayed performance tests. Proceedings of the National Academy of Sciences, 93(24), 13487?13493. doi: 10.1073/pnas.93.24.13487 Hampson, R. E., Song, D., Opris, I., Santos, L. M., Shin, D. C., Gerhardt, G. A., ? Deadwyler, S. A. (2013). Facilitation of memory encoding in primate hippocampus by a neuroprosthesis that promotes task-specific neural firing. Journal of Neural Engineering, 10(6), 066013. doi: 10.1088/1741-2560/10/6/066013

Fr om t h e Br ai n t o t h e Bu t t : I t Al l St ar t s i n t h e Gu t M ichelle Pollowitz W ashington Univer sity in St. Louis '21 M ajor : Biology, M inor : Psychology Gut microbiota are the bacterial flora that exist in the stomach and intestines and affect bodily functions both in the gut and throughout the body. Some of the most important functions that microbiota carry out include metabolizing fiber into fatty acids, nourishing epithelial cells, developing the immune system, regulating hormone secretions, and detoxifying carcinogens (Klaassen & Cui, 2015). This paper highlights investigations about how microbiota affect the immune system, metabolism, and the development of neurological diseases, with a particular look at the immune system and metabolism in relation to the brain. Gut microbiota can affect an immune response occurring anywhere in the human body, including those in the brain. Gut microbiota control the production of interleukin-1? and interleukin-6 in the gut-associated lymphoid tissues. Interleukin-1? and interleukin-6 are the specific proinflammatory cytokines that predominantly affect the brain. Proinflammatory cytokines are categorized as regulators of infection, but they can sometimes make the infection more dangerous, induce inflammation, and obstruct healing rather than assist the immune system in fighting the infection (Dantzer et al., 2008). These proinflammatory cytokines not only worsen the regular symptoms of a sickness, but they can also cause depressive

episodes in patients with no previous history of mental disorders. Studies have found that lipopolysaccharides and proinflammatory cytokines, such as the interleukins, increase serotonin reuptake. As more serotonin reuptake occurs and less of the neurotransmitter remains in the synaptic gap, the host presents more depressive symptoms. In addition, proinflammatory cytokines also activate the hypothalamic-pituitary-adrenal axis in the brain, which increases production of corticotropin-releasing hormone, a chemical often associated with clinical depression. Corticotropin-releasing hormone, similar to cortisol, is involved in the stress response of a host (Dantzer et al., 2008). As stress levels increase, so does the prevalence of depressive episodes (Cryan & Dinan, 2012). Thus, by inducing interleukin production, gut microbiota can provoke a series of processes that cause an increase in incidents of depression. On top of triggering chemical production and release, gut microbiota also secrete enzymes that digest soluble fibers from plant-based foods. These fibers are broken down into short-chain fatty acids (SCFAs) which are small enough to be absorbed by the intestines to use for energy. Additionally, SCFAs impact the metabolism of the host by influencing the host?s hunger and desire for food. SCFAs can bind to G protein-coupled receptors which initiate a

chain of metabolic pathways to stimulate the secretion of Peptide YY, a chemical that reduces the craving for food. Through these methods, the microbiota have the ability to alter hunger not just locally in the stomach but also in the mind (Golder & Farzi, 2014). Although gut flora are able to strongly impact the brain, they are also influenced by the brain. The brain and the gut are connected by a bi-directional network called the brain-gut axis (BGA) which includes branches of the nervous system, the endocrine system, and other message-carrying pathways. Due to the bidirectional nature of the BGA, messages relayed along the vagus nerve allow the brain to influence the gut and the gut to alter the brain (Klingelhoefer & Reichmann, 2015). The brain and microbiota communicate using peptides such as ghrelin, leptin, and Neuropeptide Y, and neurotransmitters such as dopamine, serotonin, GABA, acetylcholine, and glutamine. In relation to the BGA, the homeostasis of the gut and its microbacteria affect the hypothalamic-pituitary-adrenal axis, thus facilitating the stress response of the host (Ghaisas et al., 2016). For example, Lactobacillus helveticus and B. Longum, when combined, reduce stress-like

behavior (anxiety) and decrease stress hormones (cortisol) in animal models. On the contrary, other animal studies have shown a correspondence between gut microbiota and negative neurological conditions such as anxiety, bad moods, and pain (Cryan & Dinan, 2012). Due to the bidirectionality of the brain-gut axis, changes in the brain can also significantly impact the gut biodiversity. For example, stress can cause Irritable Bowel Syndrome, which occurs when stress signals carried along the central nervous system decrease the quantity of beneficial Lactobacillus in the gut (Cryan & Dinan, 2012). At times, gastrointestinal complications and neurological diseases can affect each other when there is a lack of microbiota regulating the brain-gut axis. Parkinson?s Disease (PD) is a neurodegenerative disorder characterized by the accumulation of the protein alpha-synuclein in the brain and other tissues (Ghaisas et al., 2016). Through interactions between neurons, alpha-synuclein spreads from the enteric nervous system to the central nervous system (Mulak & Bonaz, 2015). Over 80% of PD patients present some form of gastrointestinal dysfunction. Compared to controls, PD patients displayed a 77.6% reduction of gut Prevotellaceae which help

produce SCFAs as well as mucus to protect the lining in the gut (Scheperjans, 2015). Prevotellaceae deficiency increases the permeability of the intestines, potentially leading to antigen exposure and poor nutrient absorption (Mulak & Bonaz, 2015). Similarly, gastric ulcers, a symptom of Helicobacter pylori infection, have been associated with PD (Mulak & Bonaz, 2015). However, it has been shown that PD patients who consume L. casei bacteria have significant improvements in their gastrointestinal symptoms such as decreased abdominal pain and ulcers. The dual-directionality of the BGA allows for microbiota to affect and even induce PD, and for PD to impact gut biota.

Ref er en ces Conlon, M. A., & Bird, A. R. (2015, January). The impact of diet and lifestyle on gut microbiota and human health. Nutrients, 7(1), 17?44. doi: 10.3390/nu7010017 Cryan, J. F., & Dinan, T. G. (2012, September 12). Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour. Nature Reviews Neuroscience ,13(1), 701?712. https://doi.org/10.1038/nrn3346 Dantzer, R., O'Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008, January 01). From inflammation to sickness and depression: when the immune system subjugates the brain. Nature Reviews Neuroscience, 9(1), 46?56. https://doi.org/10.1038/nrn2297 Ghaisas, S., Maher, J., & Kanthasamy, A. (2016, February). Gut microbiome in health and disease: Linking the microbiome?gut?brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases. Pharmacology & Therapeutics. 158, 52-62. https://doi.org/10.1016/j.pharmthera.2015.11.012 Holzer, P., & Farzi, A. (2014). Neuropeptides and the microbiota-gut-brain axis. Adv Exp Med Biol. 817, 195-219. doi: 10.1007 Hur, K. Y. (2017, June 29). Gut microbiota and metabolic disorders. Diabetes Metab J. 39(3), 198-203. doi: 10.4093/dmj.2015.39.3.198. Weatherspoon, D. Inflammatory bowel disease: types, causes, and risk factors. (n.d.). https://live.staticflickr.com/8032/29872812646_f970a45864_b.jpg, Beneficial Gut Bacteria by Darryl Leja / CC BY-NC 2.0

From triggering immune responses to regulating metabolism to inducing neurological illnesses, gut bacterial flora utilize the brain-gut axis to connect and control functions throughout the body. Medications that mimic gut microbiota can decrease the prevalence of depression and stress by increasing synaptic serotonin and decreasing cortisol production (Cryan & Dinan, 2012). Though PD does not currently have a cure, drugs that eradicate Helicobacter pylori may improve motor skills in PD patients. (Mulak & Bonaz, 2015). Additionally, the incidence of PD can be controlled by implementing drugs that target and kill PD-associated microbiota. Having the perspective that the entire body is linked can help researchers to better understand the circulatory functions of the body and how all systems are interconnected. Though microscopic in size and often overlooked, gut microbiota play a large role in how we think and feel.

Th e Ef f ect of Tr au m at i c Br ai n I n ju r y on Fear An abel l e Pau l in o H ar var d College '21 M ajor : N eur oscience

Th e lon g-last in g ef f ect s of t r au m at ic br ain in ju r y (TBI) ar e n ot lim it ed t o ph ysical im pair m en t s. Psych ological alt er at ion s can be seen as a r esu lt of TBI, su ch as in t h e case of Ph in eas Gage, w h o u n der w en t a dr am at ic sh if t in per son alit y as a r esu lt of h is f r on t al lobe in ju r y. I am in t er est ed, t h u s, in in vest igat in g ef f ect s of t r au m at ic n eu r ological in ju r ies on f ear , an em ot ion w it h w idely-st u died ph ysical an d em ot ion al f acet s. Th is r eview st u dies t h is ef f ect of t r au m at ic n eu r ological in ju r ies on f ear in a m u lt if acet ed m an n er , look in g at f eat u r es su ch r ecogn it ion an d lear n in g. Em ot ion al r ecogn it ion is over all im pair ed by TBI (Celegh in et al., 2019; Visser -Keizer et al., 2016; Rosen ber g et al., 2015). Celegh in et al. (2019) in vest igat ed t h is by im plem en t in g bot h a n eu r opsych ological assessm en t an d an exper im en t al t ask , w h er e pat ien t s m u st discr im in at e am on g black an d w h it e f aces of sever al em ot ion s, in clu din g f ear . Th e im pair m en t seen in em ot ion al r ecogn it ion w as especially exacer bat ed f or n egat ive expr ession s (Celegh in et al., 2019; Rosen ber g et al., 2015). Rosen ber g et al. (2015) decided t o t ake t h is in vest igat ion on e st ep f u r t h er , an d in vest igat ed t h e dif f er en ce bet w een em ot ion al r ecogn it ion w h en st im u li ar e at 100% in t en sit y ver su s w h en

t h ey ar e equ at ed on in t en sit y. Th ey did t h is in or der t o at t em pt t o balan ce ou t h ow dif f icu lt it m ay be t o det ect cer t ain em ot ion s as opposed t o ot h er s (Rosen ber g et al., 2015). Wit h bot h m easu r es, t h e TBI gr ou p w as f ou n d t o be w or se at over all em ot ion r ecogn it ion t h an t h e con t r ols (Rosen ber g et al., 2015). How ever , on ce delin eat ed in t o ?f u ll-blow n? ver su s ?equ at ed? m easu r es, t he r esu lt s dif f er ed. Given ?f u ll-blow n? f acial st im u li, in dividu als w it h TBI w er e sh ow n t o be select ively im pair ed in r ecogn izin g n egat ive em ot ion s su ch as f ear (Rosen ber g et al., 2015), w h ich is con sist en t w it h r esu lt s seen in bot h Celegh in et al. (2019) an d Visser -Keizer et al. (2016), bu t given f acial st im u li t h at ar e equ at ed f or in t en sit y of expr ession , TBI par t icipan t s did n ot sh ow a gr eat er im pair m en t in r ecogn izin g n egat ive em ot ion s, an d in st ead sh ow ed a gen er al im pair m en t at r ecogn izin g em ot ion s (Rosen ber g et al., 2015). Visser -Keizer et al. (2016) looked at f ear r ecogn it ion in t h e con t ext of decision m ak in g. Th ey h ypot h esized t h at bet t er abilit y t o r ecogn ize f ear is r elat ed t o r egu lat ion of r isk beh avior , an d t h at pat ien t s w it h TBI w ou ld be w or se at bot h f ear r ecogn it ion an d af f ect ive decision m ak in g t h an t h eir h ealt h y con t r ol

cou n t er par t s (Visser -Keizer et al., 2016). As pr edict ed, bot h f ear r ecogn it ion an d decision m ak in g w er e sign if ican t ly im pair ed in TBI pat ien t s com par ed t o h ealt h y con t r ols. Th e r esu lt s, in t er m s of f ear r ecogn it ion , w er e con sist en t w it h Rosen ber g et al. (2016) an d Celegh in et al. (2019), an d pr ovided an in t er est in g applicat ion f or t h e ef f ect of im pair ed f ear r ecogn it ion . TBI is associat ed w it h ch an ges in f ear lear n in g, especially in t er m s of f ear ext in ct ion , or (Glen n et al., 2017; Zh ao et al., 2018). Zh ao et al. (2018) an alyzed t h ese ch an ges t h r ou gh a pr im ar ily cellu lar view poin t in or der t o in vest igat e t h e cellu lar m ech an ism (s) t h at u n der lie r epor t ed com or bidit y bet w een TBI an d st r ess-r elat ed disor der s. In t h eir exper im en t , t h ey f ou n d t h at t h eir TBI m odel im pair ed bot h con t ext f ear ext in ct ion an d m em or y of ext in ct ion in r at s (Zh ao et al., 2018). In ot h er w or ds, r at s w h o u n der w en t t h e TBI m odel gen er ally h ad a h ar der t im e w it h f or get t in g con dit ion ed f ear r espon ses. Th r ou gh m or ph ological ch an ges of n eu r on s in t h e in f r alim bic (IL) cor t ex as a r esu lt of TBI, IL cor t ex f u n ct ion m ay h ave been com pr om ised, m ak in g a per son m or e su scept ible t o st r ess-r elat ed disor der s by im pair in g ext in ct ion lear n in g an d/ or ext in ct ion m em or y (Zh ao et al. 2018). In t er m s of ext in ct ion lear n in g im pair m en t s, an im als w it h TBI sh ow ed poor ext in ct ion lear n in g an d in cr eased f r eezin g com par ed t o sh am -oper at ed, in dicat in g poor m em or y of ext in ct ion as w ell (Zh ao et al., 2018). In t er est in gly en ou gh , Sier r a-M er cado et al. (2015) sh ow ed t h e opposit e. Wit h t h eir TBI m odel in m ice, t h er e w as n o ef f ect on eit h er t h e

acqu isit ion or expr ession of f ear an d ext in ct ion m em or ies (Sier r a-M er cado et al., 2015), w h ich is con t r ar y t o w h at t h ey h ad pr edict ed. How ever , Sier r a-M er cado et al. (2015) advise cau t ion w h en in t er pr et in g t h ese r esu lt s, as it is possible t h at dif f er en t TBI m odels af f ect f ear -lear n in g cir cu it r y dif f er en t ly, an d t h u s can sh ow var yin g r esu lt s. Un like Sier r a-M er cado et al. (2015) an d Zh ao et al. (2018), Glen n et al. (2017) f ocu sed on h u m an par t icipan t s in t h eir in vest igat ion of t h e pot en t ial ef f ect of TBI on f ear lear n in g an d ext in ct ion . Over all, t h ey f ou n d t h at TBI is associat ed w it h alt er at ion s in t h e n eu r al cir cu it r y u n der lyin g f ear lear n in g, specif ically in f ear acqu isit ion , expr ession , an d ext in ct ion (Glen n et al., 2017). Th is is con sist en t w it h t h e r esu lt s seen in Zh ao et al. (2018). Addit ion ally, con dit ion ed f ear m ay be exacer bat ed by exper ien cin g m u lt iple TBI w it h in a 2- t o 3-year t im e f r am e (Glen n et al., 2017). Th e f in din gs f r om t h is can be con n ect ed t o t h e u n der lyin g et iology of psych iat r ic disor der s su ch as PTSD (Glen n et al., 2017). Over all, t h is r eview discu sses t h e ef f ect of TBI on f ear . It does so t h r ou gh var iou s len ses, look in g at t h e ef f ect on TBI on bot h f ear r ecogn it ion an d lear n in g. Wh ile em ot ion al r ecogn it ion , on t h e w h ole, is n egat ively af f ect ed by TBI, t h er e is som e disagr eem en t on w h et h er or n ot t h e r ecogn it ion of n egat ive em ot ion s, su ch as f ear , ar e specif ically m or e im pair ed. TBI is gen er ally also sh ow n t o be con n ect ed t o ch an ges in f ear lear n in g, specif ically in t er m s of f ear ext in ct ion m em or y, alt h ou gh t h is ef f ect is var iable in t h e exper im en t s m en t ion ed above.

Alt h ou gh t he r esu lt s ar e pot en t ially con t r adict or y at t im es, t h e exist in g r esu lt s sh ow pr om ise f or u n der st an din g h ow em ot ion s ar e pr ocessed in t h e con t ext of ph ysiological in ju r y. Upon lear n in g m or e abou t h ow t r au m at ic n eu r ological in ju r ies af f ect em ot ion s su ch as f ear , w h ich can be t ied t o psych iat r ic disor der s su ch as an xiet y an d PTSD, clin ical in t er ven t ion s can be pu t in t o place t o h elp m it igat e an d t r eat t h ese disor der s. Addit ion ally, t h e an alysis of em ot ion al beh avior al ch an ges af t er TBI can be con n ect ed t o ot h er f acet s of cogn it ion su ch as decision -m ak in g, w h ich w as m en t ion ed above as bein g con n ect ed t o f ear . St u dyin g h ow em ot ion af f ect s cogn it ion is im por t an t f or pr edict in g beh avior , an d pr ovidin g pot en t ial an t icipat or y t r eat m en t , af t er t r au m at ic n eu r ological in ju r y. Ref er en ces Celeghin, A., Galetto, V., Tamietto, M., & Zettin, M. (2019). Emotion Recognition in Low-Spatial Frequencies Is Partly Preserved following Traumatic Brain Injury. BioMed Research International, 2019, 1?10. https://doi.org/10.1155/2019/9562935 Glenn, D. E., Acheson, D. T., Geyer, M. A., Nievergelt, C. M., Baker, D. G., Risbrough, V. B., & MRS-II Team. (2017). Fear learning alterations after traumatic brain injury and their role in development of posttraumatic stress symptoms: GLENN et al. Depression and Anxiety, 34(8), 723?733. https://doi.org/10.1002/da.22642 Rosenberg, H., Dethier, M., Kessels, R. P. C., Westbrook, R. F., & McDonald, S. (2015). Emotion perception after moderate?severe traumatic brain injury: The valence effect and the role of working memory, processing speed, and nonverbal reasoning. Neuropsychology, 29(4), 509?521. https://doi.org/10.1037/neu0000171 Sierra-Mercado, D., McAllister, L. M., Lee, C. C. H., Milad, M. R., Eskandar, E. N., & Whalen, M. J. (2015). Controlled cortical impact before or after fear conditioning does not affect fear extinction in mice. Brain Research, 1606, 133?141. https://doi.org/10.1016/j.brainres.2015.02.031 Visser-Keizer, A. C., Westerhof-Evers, H. J., Gerritsen, M. J. J., van der Naalt, J., & Spikman, J. M. (2016). To Fear Is to Gain? The Role of Fear Recognition in Risky Decision Making in TBI Patients and Healthy Controls. PLOS ONE, 11(11), e0166995. https://doi.org/10.1371/journal.pone.0166995 Zhao, J., Huynh, J., Hylin, M. J., O?Malley, J. J., Perez, A., Moore, A. N., & Dash, P. K. (2018). Mild Traumatic Brain Injury Reduces Spine Density of Projection Neurons in the Medial Prefrontal Cortex and Impairs Extinction of Contextual Fear Memory. Journal of Neurotrauma, 35(1), 149?156. https://doi.org/10.1089/neu.2016.4898 Chromolithograph by A. Schmitson / Public Domain

Tr eat i n g Par k i n son ?s Di sease: Cu r r en t St at e of t h e Ar t An vita Ku l sh r esth a Univer sity of Califor nia, Ber keley '21 M ajor : M olecular and Cellular Biology and N utr itional Sciences Parkinson?s Disease (PD) is the second most common neurodegenerative disorder worldwide (Lin et al., 2019). It is characterized by tremors, impaired balance, loss of motor control, and sometimes dementia. On a molecular level, it is caused by the degradation of specialized neurons in a brain region called substantia nigra, which is responsible for motor control. These neurons produce dopamine, one of the most important neurotransmitters in the body. Due to the death of dopaminergic neurons, most body movements are greatly hampered. Recent evidence suggests that a protein called ?-synuclein aggregates in Lewy bodies, which plays a key role in the progression of the disease. The remainder of this article summarizes the state of the art in identifying hallmarks of PD using both structural and molecular pathologies. PD was first recognized as a medical condition in 1817 when English surgeon James Parkinson described it in his work, An Essay on the Shaking Palsy. He recognized that the disease is of long duration and hence requires constant monitoring of the same subject from the

onset of the symptoms till its last stages (Parkinson, 2002). Later, this condition was named Parkinson?s Disease by Jean-Martin Charcot. Even after more than two centuries, our knowledge about the disease is still limited, and we have not been able to treat it completely. In the process, however, scientists have identified key structural and molecular pathologies that are present in more than 90% of PD cases. It was initially hypothesized that only the dopaminergic neurons of substantia nigra were affected by this medical condition. Later, this theory was proved wrong by Braak and his colleagues when they proposed a Lewy-pathology based model wherein the different stages of the disease were linked to different regions of the brain (Braak et al., 2003). The neuronal damage is not random but instead follows a pre-determined path marked by characteristic changes in topography (Braak et al., 2003). Stages 1 & 2 are confined to medulla oblongata (dorsal IX/X motor nucleus & th e immediate reticular zone). Stage 3 is restrained to the lower and upper brain stem in the absence of cortical lesions, and some initial affection of the anteromedial

temporal mesocortex can be observed in Stage 4. As it progresses to later stages (Stage 5 and 6), almost the entire brain is involved, including the neocortical areas (Braak et al., 2003). This theory provided a clear pathway of the degradation of neurons and increased speculations amongst the scientific community about controlling the damage at various stages. Furthermore, PD patients with mild cognitive impairment (MCI) develop dementia and have co-morbid symptoms such as visual hallucinations. Coordinate based network mapping has revealed that the correlates of visual hallucinations and that of MCI map onto different locations in the brain, distinct from the hippocampal network of Parkinson?s dementia (Weil et al., 2019). However, to understand the key players involved in the process and identify potential drug targets, it is important to study the molecular pathologies. The pathogenesis of PD is a multifactorial process, with the primary contributors known to be age, environment, and genetic factors (Lin et al., 2019). One of the hallmarks of PD is the accumulation of presynaptic protein, ?-synuclein, which plays an important role in vesicle trafficking and endocytosis. Increased oxidative stress leads to ?-synuclein accumulation as it impairs the ubiquitin-proteasome system responsible for degrading misfolded protein. Therefore, mitochondrial dysfunction, disruption of network integrity, and ?-synuclein accumulation are responsible at the molecular level for reducing the brain?s neurogenic plasticity. According to Lin et al., both mitochondria and endo-lysosomal dysfunction contribute to the development of ?-synuclein pathology. Based on the highly variable clinical presentation among PD patients, the specific organelle playing the most important role may be moderated by individual genetic and environmental factors.

just increasing the dopamine concentration in the brain or a combination of modulating other enzymes along with increasing dopamine, thereby increasing the quality of life of the patients (Zhang et al., 2016). No cure has yet been identified, but as with most therapies, these drugs have many detrimental side effects. A new approach, the Personalized Parkinson Project, involves examining disease progression through monitoring broad biomarkers (Bloem et al., 2019). This may prove beneficial in understanding differences in pathophysiology and phenotypic diversity, which in turn can lead to highly specific treatments. In general, research advances in identifying other PD-related proteins and biomarkers may lead to potential drug targets (Zhang et al., 2016). Emerging technologies like genomics and chemoproteomics may provide an alternative drug development path. Further research in identifying targets is required for effective treatment of Parkinson?s Disease. Ref er en ces Bloem, B. R., Marks, W. J., Silva de Lima, A. L., Kuijf, M. L., van Laar, T., Jacobs, B. P. F., Verbeek, M. M., Helmich, R. C., van de Warrenburg, B. P., Evers, L. J. W., intHout, J., van de Zande, T., Snyder, T. M., Kapur, R., & Meinders, M. J. (2019). The Personalized Parkinson Project: Examining disease progression through broad biomarkers in early Parkinson?s disease. BMC Neurology, 19(1), 160. https://doi.org/10.1186/s12883-019-1394-3 Braak, H., Tredici, K. D., RĂźb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003). Staging of brain pathology related to sporadic Parkinson?s disease. Neurobiology of Aging, 24(2), 197?211. https://doi.org/10.1016/S0197-4580(02)00065-9 Lin, K.-J., Lin, K.-L., Chen, S.-D., Liou, C.-W., Chuang, Y.-C., Lin, H.-Y., & Lin, T.-K. (2019). The Overcrowded Crossroads: Mitochondria, Alpha-Synuclein, and the Endo-Lysosomal System Interaction in Parkinson?s Disease. International Journal of Molecular Sciences, 20(21). https://doi.org/10.3390/ijms20215312 Parkinson, J. (2002). An Essay on the Shaking Palsy. JNeuropsychiatry Clin Neurosci, 14. Weil, R. S., Hsu, J. K., Darby, R. R., Soussand, L., & Fox, M. D. (2019). Neuroimaging in Parkinson?s disease dementia: Connecting the dots. Brain Communications, 1(1), fcz006. https://doi.org/10.1093/braincomms/fcz006 Zhang, H., Tong, R., Bai, L., Shi, J., & Ouyang, L. (2016). Emerging targets and new small molecule therapies in Parkinson?s disease treatment. Bioorganic & Medicinal Chemistry, 24(7), 1419?1430. https://doi.org/10.1016/j.bmc.2016.02.030 Image by Malyszkz / Public Domain

Current drug treatment for PD centers around either

Cogn i t i v e Beh av i or al Th er ap y f or t h e Tr eat m en t of Per i n at al Dep r essi on Bail ey Sal im es Boston Univer sity '22 M ajor : N eur oscience A woman?s mental and physical state through pregnancy?prenatal and postnatal?differs extremely from person to person. Some women continue with their usual lifestyles, while others suffer tremendously from the hormonal and physical changes surging through their bodies. Roughly 10-15% of women experience some sort of depression during pregnancy, rendering it very common (Cuijpers et al., 2007; Sokol et al., 2011). Cognitive behavioral therapy (CBT) has become one of the most widely used therapies for the treatment of many mental illnesses, and the treatment of perinatal depression is no exception (NACBT, 2016). CBT is an umbrella term for many types of cognitive therapies that have similar approaches. Therapies with the methodology of CBT emphasize how people?s emotions and thoughts are what determine people?s actions, behaviors, and reactions. Psychologists using CBT strive to improve maladaptive behaviors by decreasing emotional or psychological stress in the clients or patients (NACBT, 2016). CBT can be useful in treating and preventing perinatal depression, along with other disorders that often occur during pregnancy, because it allows the woman to feel more positively about her behavior and situation rather than dwell on her body?s natural adaptations to pregnancy. Research over the past several years has shown that

psychological treatment for perinatal depression has been not only effective but also preventative when started in the early stages of a woman?s pregnancy (Sokol et al., 2011). Because of the concerns with antidepressants and other drugs interfering with the development of a fetus, or the potential negative outcomes when the child is born, therapy is an alternative form of treatment for these women (Sokol et al., 2011). In addition, some doctors and therapists administering CBT can adapt to individual situations (Sokol, 2015). Programs that allow for in-home, online, or in-clinic sessions allow for a more relaxed and flexible schedule for the patients. Prenatal CBT exposes women to therapy prior to giving birth, so they may feel more relaxed about the idea of psychotherapy postpartum if needed. In a meta-analysis of treatments for perinatal depression by Sokol, Epperson, and Barber (2011), they discuss the benefits of CBT and other behavioral therapies over prescribed medications. In general, women preferred psychological treatment over antidepressants (Sokol et al., 2011). A wide variety of neuropsychological-related issues can arise from prenatal depression, such as lower cortisol, serotonin, and dopamine levels along with trouble sleeping and increased anxiety (Field et al., 2010). The many varieties of CBT have been known

to help patients think through their emotions and create positive thoughts around what is changing in their lives. Along with preventing and treating prenatal depression, CBT has been known to effectively treat postpartum depression (Sokol, 2015). According to the DSM-5 (2013), 3-6% of women will have a major depressive episode at some point in their pregnancy (American Psychiatric Association, 2013). Of these women who have major depressive episodes, roughly 1 in 750 women will have postpartum psychotic episodes along with depression. Symptoms of postnatal depression may include, but are not limited to, feelings of sadness, guilt, confusion, anxiety, and sometimes even suicidal thoughts (Huang et al., 2018). It is important for physicians and psychologists to discuss CBT with their patients and clients. Taking some antidepressants, such as monoamine oxidase inhibitors and tricyclic antidepressants, can improve the symptoms of postpartum depression but may have an impact on the baby through milk metabolism (Huang et al., 2018). Clinicians have recognized the importance of integrating therapy into the postpartum depression treatment plan. While therapists are widely available to help a patient through perinatal CBT, midwives also often play a key role in the birthing process for women. Midwives who are present in pre- or postnatal care should also consider learning some techniques of CBT because the women they care for may be more receptive to their midwives than new therapists. The quality of life for the mother and new child can be significantly improved through the proper use of postpartum CBT rather than the use of medications (or sometimes a combination of the two) (Sokol,

2015; Huang et al., 2018). Overall, CBT is an effective, medication-free form of treatment for perinatal depression. A doctor or therapist can use CBT to help prenatal or postpartum depression patients overcome their fears, negative thoughts, overwhelming feelings of sadness, and other stressful symptoms. Talking with women and seeing how they are doing on an emotional level, and tackling treatment from there, has proven to be more effective and more accepted by the perinatal community (Sokol, 2015; Sokol et al., 2011). Women who are struggling with depression before or after pregnancy should consider adding forms of CBT to their treatment plan so they can use a thought-provoking approach to healing.

Ref er en ces American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.) https://doi.org/10.1176/appi.books.9780890425596 Cuijpers, P., Brannmark, J. G., & van Straten, A. (2007). Psychological Treatment of Postpartum Depression: A Meta-Analysis. Journal of Clinical Psychology, 64(1), 103?118. doi: 10.1002/jclp.20432 Field, T., Diego, M., & Hernandez-Reif, M. (2010). Prenatal depression effects and interventions: A review. Infant Behavior and Development, 33, 409?418. doi: 10.1016/j.infbeh.2010.04.005 Huang, L., Zhao, Y., Qiang, C., & Fan, B. (2018). Is cognitive behavioral therapy a better choice for women with postnatal depression? A systematic review and meta-analysis. Plos One, 1?16. doi: 10.1371/journal.pone.0205243 Sokol, L. E., Epperson, C. N., & Barber, J. P. (2011). A meta-analysis of treatments for perinatal depression. Clinical Psychology Review, 31, 839?849. doi: 10.1016/j.cpr.2011.03.009 Sokol, L. E. (2015). A systematic review of the efficacy of cognitive behavioral therapy for treating and preventing perinatal depression. Journal of Affective Disorders, 177, 7?21. doi: 10.1016/j.jad.2015.01.052 What is Cognitive-Behavioral Therapy (CBT)? (2016, May 16). Retrieved April 2, 2020, from https://www.nacbt.org/whatiscbt-htm/

Br ai n Si gn al Com p l ex i t y Ch r istoph er H al l Univer sity of Vir ginia '20 M ajor : Statistics and Cognitive Science An announcement is made over the intercom in a busy subway and is barely audible. Going through old family albums, faces and relatives are nearly unrecognizable in the antique and grainy photographs. These challenges in signal detection are due to extra noise or variability that complicates and conceals signals useful for making decisions. Often times, the desire of research is to find the signals and trends that are obscured by variability. In brain imaging studies, signal noise is often considered an artifact to be filtered out. However, recent research suggests that brain signal complexity is a meaningful property of the brain that should be measured and studied (Garrett et al., 2013). Noise may play a nonintuitive functional role for the brain in various tasks, as increased noise is correlated with higher accuracy and faster reaction times (Garrett et al., 2013). Possible reasons for these benefits of noise have already been discovered in other fields such as physics and engineering. Some examples are increased resilience to signal variability (Basalyga & Salinas, 2006), greater efficiency (Garrett et al., 2013; McDonnell & Ward, 2011) and better calculations through annealing (Faisal, Selen, & Wolpert, 2009). One measure of brain signal complexity is entropy. In short, entropy is the amount of disorder and/or complexity in a system. Entropy is more useful than

other traditional measures of variability such as signal deviation as it measure the predictability of a signal and not just the variability or distributional width (Grundy, Barker, Anderson, & Shedden, 2019). Highly unpredictable, random signals are assigned a high value of entropy, whereas predictable, regular signals are assigned a low value of entropy. An example given by Pincus, Gladstone, & Ehrenkranz, (1991) explains the importance of this measure compared to standard deviation. Suppose that person A?s heart rate fluctuates between 70 and 90 at regular intervals. Now imagine that person B?s heart rate also fluctuates between 70 and 90 but at irregular intervals. Both person A and person B will have the same mean and standard deviation. However, there is clearly some difference and it has been shown that person B?s heart rate is more indicative of a healthy heart (Pincus et al., 1991). Entropy, unlike other variability measurements, can differentiate between the two. There are multiple algorithms available for the calculation of entropy. Multiscale entropy (MSE) is considered the current gold standard, as it is able to differentiate between time scales. This is wonderfully elucidating as, when applied to neural data, fine timescales are associated with local processing, while coarse timescales are associated with distributed networks (Von Stein & Sarnthein, 2000).

MSE in patient populations has been helpful in further understanding the mechanisms of several ailments. For example, Traumatic Brain Injury (TBI) patients overall had lower signal complexity than their peers as found by doctors Raja Beharelle, Kovacevic, McIntosh, & Levine (2012). The lower complexity may indicate that connections in parts of the brain that are contributing to the noise in healthy controls are not contributing in the TBI patients. MSE has also been applied in mental disorder research such as schizophrenia, autism spectrum condition (ASC), and Alzheimer ?s Disease (Bosl, Tierney, Tager-Flusberg, & Nelson, 2011; Fernรกndez, Gรณmez, Hornero, & Lรณpez-Ibor, 2013; Takahashi, 2013; Takahashi (2013) for review). As those with ASC have lower behavioral flexibility, it was expected and found that they also have lower values of MSE (Bosl et al., 2011; Catarino, Churches, Baron-Cohen, Andrade, & Ring, 2011). These findings are likely related to the known atypical network connectivity found in those with ASC. Not only is this a beautiful example of hypothesized theories being confirmed using a new method, but these differences were also not found in power spectra analysis, indicating the usefulness of studying entropy specifically (Milne, Scope, Pascalis, Buckley, & Makeig, 2009; Raymaekers, Wiersema, & Roeyers, 2009). Although most other pathologies seem to indicate a decrease in brain signal complexity, schizophrenia research has shown both an increase and decrease in complexity in schizophrenic patients compared to controls. One particular study (Takahashi et al., 2010) found that at the onset of schizophrenic symptoms there was increased complexity as measured by MSE and, several weeks after treatment, there was a general decrease in complexity as measured by MSE.

Theoretically, schizophrenia is characterized with abnormal neuronal firing and synchronization implying greater signal complexity. As medication decreases symptoms, the unpredictable and troublesome neuronal firing decreases. Maturation appears to lead to a brain with greater functional variability, which is indicative of enhanced neural complexity. This finding could explain the known fact that adults perform more accurately, faster, and with less variation than children on tasks. The correlation between MSE and task performance or speed is diminished when controlling for the age of the participant. This indicates that the correlation effects of MSE are maturational and show the brain learning to work (McIntosh, Kovacevic, & Itier, 2008). One of the explanations for the increase in MSE in adults is that more brain areas contribute to the task at hand. Intuitively, as one ages, one comes across more and different kinds of information. Thus, more brain areas may have relevant information for any given stimulus contributing to the overall orchestra of different signals. This explanation hinges on increased knowledge or familiarity with a stimulus correlating with increased values of MSE. This was tested and found to be the case (Heisz, Shedden, & McIntosh, 2012). Those results also lead to the refinement of several proposed neural mechanisms of learning (Heisz et al., 2012). Overall, brain signal complexity is fascinating new aspect of the mind that researchers can appreciate. The refinement of neural mechanisms influencing altered behavior and discovering new models of learning in children are good and useful, but this new tool does something more. Researching brain signal complexity fosters collaboration in the

scientific community. Other fields have answers to questions that can now be applied to the brain, bringing experts in different fields into the same conversation. Communication breeds collaboration, leaving the world a richer environment to explore and our brains wonderfully more complex.

Psychiatry, 45, 258?266. https://doi.org/10.1016/j.pnpbp.2012.05.001 Takahashi, T., Cho, R. Y., Mizuno, T., Kikuchi, M., Murata, T., Takahashi, K., & Wada, Y. (2010). Antipsychotics reverse abnormal EEG complexity in drug-naive schizophrenia: A multiscale entropy analysis. NeuroImage. https://doi.org/10.1016/j.neuroimage.2010.02.009 Von Stein, A., & Sarnthein, J. (2000). Different frequencies for different scales of cortical integration: From local gamma to long range alpha/theta synchronization. International Journal of Psychophysiology. https://doi.org/10.1016/S0167-8760(00)00172-0

Ref er en ces

Basalyga, G., & Salinas, E. (2006). Robustness to Synaptic Noise. Neural Computation, 1379, 1349?1379. Bosl, W., Tierney, A., Tager-Flusberg, H., & Nelson, C. (2011). EEG complexity as a biomarker for autism spectrum disorder risk. BMC Medicine, 9(1), 18. https://doi.org/10.1186/1741-7015-9-18 Catarino, A., Churches, O., Baron-Cohen, S., Andrade, A., & Ring, H. (2011). Atypical EEG complexity in autism spectrum conditions: A multiscale entropy analysis. Clinical Neurophysiology, 122(12), 2375?2383. https://doi.org/10.1016/j.clinph.2011.05.004 Faisal, a A., Selen, L. P. J., & Wolpert, D. M. (2009). UKPMC Funders Group Noise in the nervous system. Learning, 9(4), 292?303. https://doi.org/10.1038/nrn2258.Noise Fernรกndez, A., Gรณmez, C., Hornero, R., & Lรณpez-Ibor, J. J. (2013). Complexity and schizophrenia. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 45, 267?276. https://doi.org/10.1016/j.pnpbp.2012.03.015 Garrett, D. D., Samanez-Larkin, G. R., MacDonald, S. W. S., Lindenberger, U., McIntosh, A. R., & Grady, C. L. (2013). Moment-to-moment brain signal variability: A next frontier in human brain mapping? Neuroscience and Biobehavioral Reviews. https://doi.org/10.1016/j.neubiorev.2013.02.015 Grundy, J. G., Barker, R. M., Anderson, J. A. E., & Shedden, J. M. (2019). The relation between brain signal complexity and task difficulty on an executive function task. NeuroImage, 198(December 2018), 104?113. https://doi.org/10.1016/j.neuroimage.2019.05.045 Heisz, J. J., Shedden, J. M., & McIntosh, A. R. (2012). Relating brain signal variability to knowledge representation. NeuroImage. https://doi.org/10.1016/j.neuroimage.2012.08.018 McDonnell, M. D., & Ward, L. M. (2011). The benefits of noise in neural systems: Bridging theory and experiment. Nature Reviews Neuroscience, 12(7), 415?425. https://doi.org/10.1038/nrn3061 McIntosh, A. R., Kovacevic, N., & Itier, R. J. (2008). Increased brain signal variability accompanies lower behavioral variability in development. PLoS Computational Biology, 4(7). https://doi.org/10.1371/journal.pcbi.1000106 Milne, E., Scope, A., Pascalis, O., Buckley, D., & Makeig, S. (2009). Independent Component Analysis Reveals Atypical Electroencephalographic Activity During Visual Perception in Individuals with Autism. Biological Psychiatry. https://doi.org/10.1016/j.biopsych.2008.07.017 Pincus, S. M., Gladstone, I. M., & Ehrenkranz, R. A. (1991). A regularity statistic for medical data analysis. Journal of Clinical Monitoring. https://doi.org/10.1007/BF01619355 Raja Beharelle, A., Kovacevic, N., McIntosh, A. R., & Levine, B. (2012). Brain signal variability relates to stability of behavior after recovery from diffuse brain injury. NeuroImage, 60(2), 1528?1537. https://doi.org/10.1016/j.neuroimage.2012.01.037 Raymaekers, R., Wiersema, J. R., & Roeyers, H. (2009). EEG study of the mirror neuron system in children with high functioning autism. Brain Research. https://doi.org/10.1016/j.brainres.2009.09.068 Takahashi, T. (2013). Complexity of spontaneous brain activity in mental disorders. Progress in Neuro-Psychopharmacology and Biological

Th e M ed i a Con t r ol l i n g t h e Un d er l y i n g N eu r ol ogi cal Cau se of Bu l i m i a In du m ath i Pr ak ash H ar var d College '22 M ajor : M olecular and Cellular Biology Bulimia is one subset of all the eating disorders that are prevalent throughout the world. This disorder affects millions of people worldwide and it is crucial to find a way to lower the numbers. The psychological factors of bulimia, such as perfectionism, contribute to neurological changes in dopamine which causes a nonstop circle of recurring bulimic symptoms including binging and purging. The neurological causes of bulimia are crucial to understand because the environment triggers psychological factors of a disorder to arise which are also interconnected to neurons and neurotransmitters. For instance, in bulimia, there are many neurotransmitters related to the behaviors that define the disorder. One such chemical change is the increase of the peptide YY in cerebrospinal fluid. This increase in YY is one of the driving causes of the binging behavior that bulimic patients exhibit, causing this binging to be uncontrollable and impulsive (Kaye & Weltzin, 1991). Another such chemical change in bulimia nervosa is a disruption in the secretion of cholecystokinin which is a peptide that regulates food intake for a human by increasing the satisfactory feeling from eating which thus reduces excessive food intake (Kaye & Weltzin, 1991). Hence, these two chemical imbalances are huge causes of

binging in bulimic patients. On a similar note, it is proven that women with bulimia have serotonin, norepinephrine, and dopamine levels that are altered (Broft, Berner, Martinez, & Walsh, 2011). Related to the dopamine reward system, bulimia is comorbid with addiction. Thus, the neurological system dysfunction of addiction is similar to that of bulimia. The dopamine reward system is also related to motivation. The brain has survival behaviors like eating and drinking that are related to the dopamine reward system (Broft, Berner, Martinez, & Walsh, 2011). When there is a reward, there is a change in the circuitry that causes the human body to act motivationally in those behaviors that cause the reward. This works through the release of dopamine in the nucleus accumbens, a brain region located within the ventral striatum. Dopamine is what is involved in the feeling of pleasure, but even more crucially, it is involved with the motivation one feels (Broft, Berner, Martinez, & Walsh, 2011). Thus, when there is a hint of something being a reward, there is dopamine released in the nucleus accumbens, allowing the body to obtain the reward. Neurochemistry is a huge contributing factor in bulimia as there is a cycle where harmful standards perpetuated by the media increase the perfectionism that one may feel. This perfectionism

then leads one to restrict their food intake to match those who have thinner, unrealistic body types. Due to genetic factors, the person has neuroticism, meaning that they may experience increased anxiety. The food restriction can, therefore, reduce the anxiety one feels as it helps them feel as if they are achieving the ideal body image (as depicted by the media). The anxiety reduction is reinforcing and stimulates increased dopamine function, which contributes to reward sensitivity that then motivates a person to continue their behavior related to bulimia. Hence, it is important to examine how body image is portrayed by the media in order to prevent this behavior from continuing. Prevalence rates are not constant throughout the world and appear to be higher in western countries when compared to non-western countries (Makino, Tsuboi, & Dennerstein, 2004). The reason for this difference stems from how the media portrays cultural ideals of the body. It is important to identify what about culture and media can be changed to help stop the recurring cycle present in perfectionism and bulimia. The western ideal worships a thin, slender body while other non western countries embrace a larger body size and do not focus on body types as much as western countries do. Once westernization took its effect with the thin ideal portrayed more and more in non western countries, prevalence rates spiked (Bordo, 2013). Thus, to combat bulimia it would be crucial to address the thin ideal, critiquing it in order to change the attitudes of people with bulimia.

Ref er en ces Bordo, S. (2013). Unbearable weight feminism, Western culture, and the body. Berkeley, CA: Univ. of California Press. Eating Disorders: About More Than Food. (n.d.). Retrieved from https://www.nimh.nih.gov/health/publications/eating-disorders/index.shtml Kaye, W., & Weltzin, T. (1991). Neurochemistry of bulimia nervosa. The Journal of Clinical Psychiatry. Retrieved from https://europepmc.org/abstract/med/1682306. Makino, M., Tsuboi, K., & Dennerstein, L. (2004, September 27). Prevalence of eating disorders: A comparison of Western and non-Western countries. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1435625/ The Waiting Room / Bulimia Tableau by topekalibrary / CC BY-NC-SA 2.0

Ch al l en ges an d Pr osp ect s f or Cl i n i cal Ap p l i cat i on s of Rest i n g-St at e Fu n ct i on al Con n ect i v i t y Ar vin Abr am ovich Sar k issian W ashington Univer sity in St. Louis '21 M ajor : Cognitive N eur oscience The human brain is comprised of spatially distributed, functionally connected regions that exhibit spatiotemporally consistent increases and decreases in neural activity during rest. Functional magnetic resonance imaging (fMRI) has been utilized to identify predictable relationships of blood oxygen level-dependent (BOLD) activation across regions in time series data, allowing for the identification of functional connectivity networks with nodes that appear reliably within and across individuals (Beckmann et al., 2005). Whereas unique characteristics of individuals? functional connectivities are intentionally ignored in many comparative studies, there is a growing mass of research concerned specifically with the identification, predictability, and explanatory power of these features on various phenotypes. Despite evidence of functional connectivity predicting various task performance and behavioral phenotypes, there has been minimal clinical utility for resting-state functional connectivity (rsFC). Though individuals? rsFC differences from population templates may not provide conclusive evidence for the presence or severity of disorder, the clinical potential of rsFC lies in its capacity to assess risk or provide supplementary diagnostic information for well-characterized disorders. If a reliable population template can be generated

specific to an individual?s expected normal, and if artifacts and noise can be removed effectively, physicians may find diagnostic value in comparing specific rsFC between pre-determined regions of interest (ROIs) within patients to those in custom population templates. By utilizing seed-map approaches to outline given ROIs and check for deviations from population templates, physicians may narrow down diagnosis options. This is especially relevant in the development of risk profiles for phenotypes with no clear structural diagnostic criteria (Paul et al., 2006), such as Alzheimer ?s, in which rsFC deviations may provide more evidence of risk or similarity to affected populations than physiological or behavioral tests can. Given the extensive literature correlating FC network traits with phenotypes, dual-regression approaches which impose prior networks onto functional data may be used to identify network-specific deficits in a standardized language of spatially consistent networks. In terms of single-subject clinical utility, however, seed-map approaches hold more promise in that they are advantageous for studies focusing on specific brain region connectivities (Smith et al., 2014). Medicine relies on individualized treatments based on individual images for patients with structural and functional irregularities that make the imposition of

a priori networks by dual-regression impractical. Therefore, physicians attempting to build better understandings of patients? deficits may benefit from seed-based findings using voxels associated with a functional area as a seed. Though data quality is a concern, physicians utilizing fMRI as a diagnostic tool can maximize reliability by increasing scanning time (Birn et al., 2012) to durations longer than those which researchers can afford, given that physicians turning to functional analysis will likely be working with one patient at a time. Though accessibility to fMRI is another concern, FC can be inferred from MEG, EEG, and other imaging methods that may be more feasible diagnostic tools for physicians with limited access. For example, FC inferred from EEG coherence is predictive of motor skill acquisition with high accuracy (Wu et al., 2014). Although this research has not concentrated on plasticity of motor functions for clinical populations, further

studies may reveal a similar predictive power of FC on motor skill plasticity that can inform a physician?s treatment or rehabilitation plan for patients, based on outcomes for previous patients with similar baseline FC deviations. This approach would benefit from the increasing availability of large datasets incorporating FC data alongside treatment outcomes longitudinally, allowing for analyses of likelihood of success for treatment options, customized by demographics and rsFC. Although there is a gap in the literature as to how inter-individual heterogeneity in FC can mechanistically underlie or predict differential plasticity, treatment plans for disorders requiring motor or cognitive rehabilitation such as traumatic brain injury or stroke are candidates for clinical application of rsFC. FC analyses conducted on resting-state data, as opposed to task-related activity, are possible for patients with varying motor and cognitive capacities; fMRI requires and benefits in terms of data quality from subjects?physical and cognitive inactivity during scanning sessions. This warrants further research as well as development of high-quality datasets inclusive of FC-inferable imaging and treatment data. While programs such as the Human Connectome Project (HCP) have

resulted in thorough characterization of both structural and functional connectivity for healthy individuals (Van Essen & Barch, 2015), there are funding opportunities for projects like the National Institutes of Health?s Connectomes Related to Human Disease that would provide more relevant data for rehabilitation-focused rsFC research. Furthermore, standardizing the data admission process into these databases can produce metrics such as clinical severity and task performance that, in cooperation with rsFC, can be utilized to customize reference statistics for individual treatments. Pre-operative mapping is another prime opportunity for clinical incorporation of rsFC. Though task-based fMRI has been utilized pre-surgery to guide neurosurgical planning (Haberg et al., 2004), it has mostly been used to identify movement and language areas in order to ensure these areas are avoided in surgery. Given that a strong concern for incorporation of fMRI in pre-surgical planning is the high inter-subject variability of structural connectivities of populations undergoing neurosurgery (Desmond & Chen, 2002), analyses of individual rsFC can be used to map custom boundaries of cortical areas non-invasively based on their rsFC, potentially minimizing the need for invasive exploratory operations to identify surgical targets. Furthermore, data converging previous operational success rates with individual rsFC characteristics can inform risk calculations for future surgeries.

functional connectivity characteristics collectively foreshadow a serious consideration of incorporating rsFC in clinical settings. The potential of using individual rsFC metrics to inform diagnostic procedures, to assemble customized risk profiles for psychiatric and neurological disorders, to predict treatment method efficacy, and to inform treatment preparation calls for more research on the optimal analysis approaches for clinically-relevant rsFC data and on the types of medical diagnoses and treatments where rsFC can be most impactful. Ref er en ces Beckmann, C. F., DeLuca, M., Devlin, J. T., & Smith, S. M. (2005). Investigations into resting state connectivity using independent component analysis. Philosophical Transactions of the Royal Society B: Biological Sciences, 360(1457), 1001-1013. Birn, R. M. (2012). The role of physiological noise in resting-state functional connectivity. Neuroimage, 62(2), 864-870. Desmond, J. E., & Chen, S. A. (2002). Ethical issues in the clinical application of fMRI: factors affecting the validity and interpretation of activations. Brain and Cognition, 50(3), 482-497. Haberg, A., Kvistad, K. A., Unsgard, G., and Haraldseth, O. (2004). Preoperative blood oxygen level-dependent functional magnetic resonance imaging in patients with primary brain tumors: clinical application and outcome. Neurosurgery, 54, 902?914. Paul, M. M., Garry, D. H., & Edward, T. M. (2006). Application of fMRI in translational medicine and clinical practice Journal of Nature Reviews. Neuroscience, Nature Publishing Group, 732-744. Smith, D. V., Utevsky, A. V., Bland, A. R., Clement, N., Clithero, J. A., Harsch, A. E., McKell Carter, R. & Huettel, S. A. (2014). Characterizing individual differences in functional connectivity using dual-regression and seed-based approaches. Neuroimage, 95, 1-12. Van Essen, D. C., & Barch, D. M. (2015). The human connectome in health and psychopathology. World Psychiatry, 14(2), 154. Wu, J., Srinivasan, R., Kaur, A., & Cramer, S. C. (2014). Resting-state cortical connectivity predicts motor skill acquisition. Neuroimage, 91. Magnetic resonance imaging of areas of the brain in the default mode network by John Graner / Public Domain

The expansion of neuroimaging data availability and accessibility, the increasingly precise processing techniques for cleaning up and making meaning of functional data, and the bank of reliable and valid associations between phenotypic traits and

Tr eating Opioid Use Disor der s Dur ing and Post-COVI D-19 Kar ina Ascunce H ar var d College '22 M ajor : N eur oscience The opioid epidemic has ravaged the United States, being declared a public health crisis in 2017 (Public Affairs, 2019). Opioid use disorder is a psychiatric illness and has diagnostic criteria outlined in the DSM-V (Saxon, 2018). 130 Americans die every day from opioid overdose on average (Centers for Disease Control and Prevention, 2020). Opioids include drugs such as heroin, codeine, morphine, and oxycodone. Prior to the COVID-19 pandemic, there existed a large gap between the number of people with opioid use disorders and those actually receiving treatment, with only 17.5 percent of people with an opioid use disorder receiving specialty treatment in 2016 (Substance Abuse and Mental Health Services Administration, 2016). This gap still exists, but the COVID-19 pandemic has exposed the ways in which we can help close it. Since the onset of this global pandemic, emergency healthcare focus has shifted towards the pressing needs of patients with COVID-19. This large-scale triage has left many patients recovering from opioid use disorder ? including those on medication-assisted treatment ? unable to have in-person visits to their local emergency departments, primary physicians, psychiatrists, and therapists. These limited services initially would have severely affected those with opioid use disorders whose experiences of stress, depression, and anxiety may heighten during this unprecedented time. Among the leading treatments for opioid use disorder are medications such as buprenorphine and

COVID-19-related restrictions on social interaction and healthcare resources have eliminated initial in-person appointments required for obtaining prescriptions, in addition to allowing patients in an Opioid Treatment Program to receive up to 28 days worth of take-home doses (Owen Gibbs, Rooney, & Tzanetakos, 2020). As such, many of the people that are reliant on medication-assisted-therapy are now finding themselves in situations where there is ?disrupted access? to the medication they need because of these COVID-19-related restrictions (National Institute on Drug Abuse, 2020). In fact, some states and counties have already seen upticks in opioidoverdose related deaths (Struett, 2020). The increase in overdoses should be enough of an incentive to streamline the process for accessing vital medications such as suboxone, methadone, or buprenorphine. Telemedicine, which allows health professionals to conduct their services through telecommunication, is a step in the right direction for reducing the daily barriers that come with treating an opioid use disorder. But ultimately, there should be a concerted effort to ensure that opioid overdose deaths, particularly in a time of low medical resources, do not continue to spike. Every effort should be made to ensure that logistical barriers, such as the lack of access to a nearby prescribing physician, do not exacerbate the gap. This means that increasing

telemedicine offerings and street outreach initiatives are necessary to implement to ensure that the most vulnerable populations have access to necessary treatment. In fact, this should be the standard, regardless of whether or not social distancing rules are in place or if there is a pandemic occurring. Before COVID-19 was declared a public health crisis, there was a law requiring an in-person visit with a physician before being able to receive a prescription for drug therapy for opioid use disorders (Levine & Wein, 2020). This law prevented many patients from receiving drug therapy, as few physicians are certified for prescribing buprenorphine, among other agonists and partial agonists like suboxone (Rapaport, 2020). These physicians who are certified have a 30-person limit on how many people they can treat with buprenorphine at a time (The National Alliance of Advocates for Buprenorphine Treatment). Underinsured and uninsured individuals, in addition to rural and homeless populations, face barriers in accessibility to doctors that are certified in prescribing

"To deny medication or make it virtually impossible to access them is inhumane." buprenorphine. Despite the federal government allowing for up to 28 days of prescription buprenorphine or methadone, people recovering from opioidopioid use disorder are facing a sharp decline in access to other resources such as safe injection and needle-exchange sites. On the flip side, the televisits and street outreach initiatives should be explored as a potential avenue for making medication-assisted-treatment more accessible to under-insured and/or uninsured, especially homeless

and socioeconomically disadvantaged, populations. To deny medication or make it virtually impossible to access them is inhumane. The COVID-19 crisis has exposed the places in which it was always a potentiality to increase access to medication. Telemedicine has the potential to reach many more patients ? the other 82.5% of people who do not get specialty treatment for their opioid use disorders. A lack of access to medication-assisted therapy during this pandemic has forced many into withdrawal and fatal overdose, but the lack of access is nothing new for those who have yet to see a physician in-person for a prescription that could save their lives. The current pandemic has forced physicians and the overall healthcare system to prove that they can do better, so now they must do better and better, for all people dealing with opioid use disorders ? and not just for those who can afford treatment. pandemic has forced physicians and the overall healthcare system to prove that they can do better, so now they must do better and better, for all people dealing with opioid use disorders ? and not just for those who can afford treatment.

Ref er ences Centers for Disease Control and Prevention. (2020, March 24). America's Drug Overdose Epidemic - Data to Action. Retrieved from https://www.cdc.gov/injury/features/prescription-drug-overdose/ index.html Levine, S. J., & Wein, E. H. (2020, April 10). COVID-19: DEA and SAMHSA Guidance for Treating Opioid Use Disorders via Telehealth. Retrieved from https://www.natlawreview.com/article/covid-19-dea-andsamhsa-guidance-treating-opioid-use-disorders-telehealth National Institute on Drug Abuse. (2016). Effective Treatments for Opioid Addiction. Retrieved from https://www.drugabuse.gov/publications/effective-treatmentsopioid-addiction/effective-treatments-opioid-addiction National Institute on Drug Abuse. (2020, April 06). COVID-19: Potential Implications for Individuals with Substance Use Disorders. Retrieved from https://www.drugabuse.gov/about-nida/noras-blog/2020/04/ covid-19-potential-implications-individuals-substance-usedisorders Photo by clarkdonald413 / Pixabay License https://storage.needpix.com/rsynced_images/drugs-4260911_1280.jpg

A ni k a Brah mbh att Boston Uni v ersi ty '23 M aj or: Psych ol ogy and M edi a Sci ence

Per su asionan d Cl im ateCh an ge (An dW h yOl der Peopl eM ay Dism issGr etaTh u n ber g)

On September 23, 2019, a sixteen-year-old girl repeatedly implored of world leaders these three poignant words: ?How dare you!? Less than thirty seconds into her speech at the United Nations Climate Action Summit, Greta Thunberg was already near tears, her voice wavering (PBS NewsHour, 2019). She went on to cite several statistical figures in her speech, while her highly emotional tone and condemnatory language persisted throughout. She called out world leaders for failing to address the climate crisis and irresponsibly leaving it in the hands of young people. Thunberg has proven effective at galvanizing thousands of young people to participate in grassroots action all over the world. However, her efforts have also drawn extreme accusations from the political right, some of whom have gone as far as to compare her to Nazi propaganda (Zraik, 2019). Of course, there is also a middle ground: adults who are conscious of climate concerns but do not necessarily see it as an urgent priority the same way many young people do. So why exactly do they respond differently from their younger counterparts to the same messages? Clearly, some of the main emotional themes conveyed through Thunberg?s U.N. speech were those of fear and loss. ?You have stolen my dreams and my childhood,? she said. ?People are

suffering. People are dying. Entire ecosystems are collapsing,? she said (NPR Staff, 2019). Yan et. al?s 2012 study regarding emotion and the persuasive effects of message framing suggests that fear and sadness can ?stimulate the [behavioral inhibition system], which will likely enhance receptivity to loss-framed appeals? (p. 697). According to this framework, Thunberg?s loss-focused messages should have been effective due to the idea of ?impending doom? induced by discussion of the climate crisis. And clearly they were, for the young people whom she prompted to take to the streets and protest legislative inaction regarding climate change. But that leaves in question those of older generations--why was her message less effective with them? Perhaps it had something to do with empathy. Younger people watching Thunberg?s speech saw a peer, a voice of their own generation. It was easy for them to feel connected to her and her message because they felt she was one of them, speaking up against the status quo imposed by older generations. Older people, even if they were sympathetic to her message, saw a child. The key difference between the two groups is that between empathy and sympathy. While empathy refers to ?[understanding] and [feeling] another 's emotions as if they were your own,? sympathy is ?[feeling] bad

for someone based on their...circumstances? (Flax, 2018). Even well-intentioned adults may subconsciously sympathize, rather than emphasize, with the emotions of young people such as Thunberg when they see a child in distress rather than a leader calling other world leaders to action. This could account for the difference between taking action and not taking action--maybe amid the intense emotion, Thunberg?s core message got lost on adults. Yan et. al.?s study discussed the implications of loss and gain-framed messages for advertisers during television programs, but there is also relevance to the world?s larger issues. For example, the finding that ?gain-framed messages should be most effective following programs that highlight perceived injustice, value-inconsistent behavior, or obstacles to goal achievement ? may imply that in general, when people are faced with a situation that they feel is difficult to overcome, gain-framed messages may be a more effective persuasion technique (p. 696). For adults who have been facing the world?s issues longer than young people, simply because they have been alive longer, combating the climate crisis may seem like a more daunting goal. Therefore, for this audience, focusing on what can be gained by taking action rather than what has been lost by resisting it

"People a r e suffer ing. People a r e dying. Entir e ecosystems a r e colla psing." -Greta Thunberg, 2019 speech at the United Nations

people, simply because they have been alive longer, combating the climate crisis may seem like a more daunting goal. Therefore, for this audience, focusing on what can be gained by taking action rather than what has been lost by resisting it would be a more effective technique to inspire change. While Thunberg?s U.N. speech was incredibly moving to those who already agreed with her ideas, a gain-framed appeal could have better persuaded people who did not already feel compelled by her Yan et. al.?s study discussed the methods. implications of loss and gain-framed messages for advertisers during Further research is needed to television programs, but there is also determine exactly how empathetic relevance to the world?s larger issues. adults can be to messages coming For example, the finding that from children. It is clear that an issue ?gain-framed messages should be such as climate change, which affects most effective following programs every living being on the planet, has that highlight perceived injustice, no reason to warrant attention only value-inconsistent behavior, or from members of a certain obstacles to goal achievement ? may generation. However, persuading imply that in general, when people are older people to take action in a faced with a situation that they feel is country where those over fifty years difficult to overcome, gain-framed old comprise more than half of the messages may be a more effective voting demographic (Lynch, 2018)--not persuasion technique (p. 696). For to mention more than three fourths of adults who have been facing the lawmakers in Congress (Morris et.al., world?s issues longer than young 2019)--may be the crucial missing link people, simply because they have to achieving drastic climate action.

Ref er ences Flax, M. (2018, July 24). The difference between empathy and sympathy (and how to nurture both). Retrieved from https://www.sacap.edu.za/blog/appliedpsychology/empathy-vs-sympathy/ Lynch, F. R. (2018, December 12). Don?t Discount Older Voters. They Could Decide the White House. The New York Times. Retrieved from https://www.nytimes.com/2018/12/12/ opinion/democrats-republicans-senior-voters -aarp-.html Morris, S., Adolphe, J., & Salam, E. (2019, June). How diverse is the 2018 US Congress? The Guardian. NPR Staff (2019, September 23). Transcript: Greta Thunberg's Speech At The U.N. Climate Action Summit. Retrieved from https://www.npr.org/2019/09/23/763452863/ transcript-greta-thunbergs-speech-at-the-u-n -climate-action-summit PBS NewsHour (2019, September 23). Watch: Greta Thunberg's full speech to world leaders at Un Climate Action Summit. Retrieved from https://www.youtube.com/watch?v=KAJsdgTPJpU Yan, C., Dillard, J. P., & Shen, F. (2012, August). Emotion, Motivation, and the Persuasive Effects of Message Framing. Retrieved from https://www.researchgate.net/publication/ 264409817_Emotion_Motivation_and_the_ Persuasive_Effects_of_Message_Framing Zraick, K. (2019, September 24). Greta Thunberg, After Pointed U.N. Speech, Faces Attacks From the Right. The New York Times. Retrieved from https://www.nytimes.com/2019/09/24/climate /greta-thunberg-un.html Sea Level Rise by npsclimatechange / Public Domain https://live.staticflickr.com/3866/142276567 90_5b2ddc8a30_b.jpg Greta Thunberg by Andy Bosselman / CC BY 2.0 https://live.staticflickr.com/65535/4888284 8248_58633b2a2f_b.jpg

Th e L i m bi c Sy st em i n L ock d ow n : W h y Ar e W e Al l Dyin g Ou r H air in Qu ar an tin e? Letizia Ye University of California, Los Angeles '20 Major: Neuroscience, Minor: Biomedical Research Despite the gloomy global lockdown, the front page of YouTube, Instagram, and many other social media sites are saturated with lively hues from millions of at-home hair coloring videos, DIY haircuts, and unfortunately, hair transformations gone wrong. With all of us sequestered in our homes for quarantine, there seems to be no better time to be focusing on some self-improvement and a little bit of personal reinvention.

Unbeknownst to the world, quarantine has united all of us in unspoken solidarity, as millions of people (myself included) have donned their masks and strolled down to their local CVS for a box of Manic Panic TM hair dye. What greeted the mirror in the aftermath of ammonia fumes, however, was either a stylish success or an embarrassing story to explain to one?s parents over FaceTime. The exponential surge in DIY transformations inspires some introspection

Fig. 1 Google Trends report on the recent worldwide increase in search popularity for hair dye

introspection as to why so many people are suddenly making such drastic alterations to their hair. Some psychologists have suggested that changing one?s physical appearance allows for individuals to exert a form of control over their lives. With a global crisis as debilitating and unpredictable as this pandemic, it is understandable that many are facing uncertainty about their futures. Interestingly, several studies demonstrate that social isolation may promote impulsive behavior and decision-making. Compounded by the stress and unease that COVID-19 presents to our familiar livelihoods, it is possible that we are only one spark away from a fiery shade of red hair. The unique circumstances of quarantine provide a compelling reason to examine the neurocircuitry underlying impulsive self-grooming. What are some of the neurological mechanisms behind self-care? How does stress hijack this circuitry and transform it into maladaptive behavior? Is it possible that social isolation exacerbates this behavior? To explore the nature of motivational and drive-related behavior, many

neuroscientists turn to the limbic system, as it contains structures that play a crucial role to regulating stress-related responses. Coincidently, there is a significant overlap between the regions that respond to stress and the ones that modulate self-grooming behavior, leading to a complex network regulated by diverse connections. Particularly, the hypothalamus has a significant role in neuroendocrine function, as the hypothalamic-pituitary-adreno (HPA) axis controls the secretion of major stress peptides, namely corticotropin-releasing hormone (CRF) and adrenocorticotropic hormone (ACTH). These have been implicated in promoting self-grooming behavior, as studies demonstrate that injections of CRF or ACTH into the lateral ventricle of rodents resulted in increased autogrooming compared to the control group (Dunn et al., 1988). Additionally, certain nuclei in the hypothalamus contribute to maintenance activity and hygiene as well. Specifically, electrical stimulation delivered via iontophoretic injections into the paraventricular nucleus or dorsal hypothalamus similarly increased self-grooming in murine models (Roeling et al., 1993). Evidently, stress-related mechanisms have a profound impact in triggering our need for self-care and personal attention and is a valid response to increased environmental pressure. However, it ?s possible that a lack of social interaction may contribute to altering the normal processes behind self-grooming. Studies conducted in isolation-reared mice show that the subjects were more likely to partake in impulsive

actions as measured by a differential reinforcement of low rates of responding (DRL) task. Here, mice were only given a reward if they were able to maintain lower rates of behavioral activity. Compared to the control group, socially isolated mice were less adept at this task, suggesting that social deprivation may be an underlying source for exacerbated spontaneous behavior (Liu et al., 2017). While limited research has been conducted on compulsive self-grooming, a ground-breaking study conducted by Hong et al. (2014) focused on the extensions of the amygdala for insights on how a traditionally comforting and restorative behavior could potentially become maladaptive. The amygdala, another critical structure in the limbic system, is heavily involved in modulating fear, anxiety, and the motivational state of individuals. By utilizing an optogenetic experimental paradigm, the team discovered specific neuronal ensembles in the medial amygdala (MeA) may control autogrooming. Subject mice expressed channelrhodopsin-2 (ChR2), a light-sensitive ion channel protein, in the glutamatergic cells of the MeA. Upon activating the ChR2-expressing cells by delivering temporally specific pulses of blue light, results show that the photostimulation resulted in almost instantaneous and repetitive self-grooming behavior that overrides previous actions. Importantly, the data revealed that mice that were alone in their home cage had a statistically significant lower onset latency and longer episodes of compulsive self-grooming in comparison to those that had a cage

mate during the experiment (Hong et al., 2014). Although it is improbable that humans will develop obsessive tendencies towards self-care, this study certainly provides unique insight as to how circuitry that modulates a natural and comforting activity could be manipulated to result in dysfunctional behavior. While quarantine is certainly a convenient time to complete that self-care bucket list or stylish makeover, it is important to be mindful of how isolation-induced stress can alter our normal behavior. Finding safe ways to reach out and connect with friends and family can help prevent the next 2 AM haircutting catastrophe. Even if your hair experiment goes awry, it ?s comforting to know that we?re all bound by some aesthetic curiosity to appreciate and love ourselves in a time when it is needed the most. Ref er ences Dunn, A. J. (1988). Studies on the Neurochemical Mechanisms and Significance of ACTH-induced Grooming. Annals of the New York Academy of Sciences, 525(1 Neural Mechan), 150?168. doi: 10.1111/j.1749-6632.1988.tb38603.x Hong, W., Kim, D.-W., & Anderson, D. J. (2014). Antagonistic Control of Social versus Repetitive Self-Grooming Behaviors by Separable Amygdala Neuronal Subsets. Cell, 158(6), 1348?1361. doi: 10.1016/j.cell.2014.07.049 Liu, Y., Wilkinson, L. S., &amp; Robbins, T. W. (2017). ?Waiting impulsivity?in isolation-reared and socially-reared rats: Effects of amphetamine. Psychopharmacology, 234(9-10), 1587-1601. doi:10.1007/s00213-017-4579-8 Massony, T. (2020, April 14). Here's Why Quarantine Hair Transformations Are Taking Over Social Media, According to Experts. Elite Daily. Roeling, T., Veening, J., Peters, J., Vermelis, M., & Nieuwenhuys, R. (1993). Efferent connections of the hypothalamic ?grooming area? in the rat. Neuroscience, 56(1), 199?225. doi: 10.1016/0306-4522(93)90574-y Hair Dye Kit by Van Hoang / CC BY 2.0 https://live.staticflickr.com/1493/ 26442149751_c6b3a29102_b.jpg

Atten tion Deficit H yper m obil ity Disor der ? Con n ectin g th e Dots Between th e Body an d th e Br ain S. Jade Barclay The University of Sydney '21 Major: Medicine / Public Health ypermobility in the body and Attention Deficit Hyperactivity Disorder (ADHD) in the brain are often found in the same person. As these two conditions are assessed, researched, and managed by different specialists, their association is frequently overlooked (Baeza-Velasco et al., 2014). ADHD frequently co-occurs with other mental health issues, substance use disorders, and sleeping problems that are routinely screened for, and comorbid musculoskeletal pain is common but is rarely screened for. Joint hypermobility is a commonly overlooked cause of pain and fatigue in 3% of the population (Kumar and Lenert, 2017). Hypermobility has been found to be present in 31.5% to 74.4% of ADHD patients in some studies, compared to 12.8% to 13.9% in healthy controls, and routine screening for joint hypermobility should be a clinical consideration (Do?an et al., 2011; Shiari et al., 2013).

Differences in brain structures have been found to be common across people with hypermobility and ADHD (Eccles et al., 2012), and delayed diagnosis in women is common in both conditions (Quinn and Madhoo, 2014). Just as the early recognition and management of ADHD has the potential to change the trajectory of an individual?s psychiatric morbidity later in life, early recognition and management of hypermobility can prevent physical disability and complex multimorbidity across the lifespan (ibid.; Mu et al., 2019). Joint hypermobility is a common yet poorly recognised connective tissue condition, including Joint Hypermobility

Syndrome (JHS) and hypermobile Ehlers-Danlos Syndrome (hEDS). Hallmark features include ligament laxity, painful joints, and slow-healing skin that stretches or bruises easily, however it affects the connective tissue in every system of the body. People with hypermobility often have a history of being clumsy or accident-prone, with frequent sprains and dislocations, and are overrepresented among those with anxiety disorders and neurodevelopmental conditions like autism and ADHD (Cederlof et al., 2016). While it is typically thought of as a musculoskeletal condition, hypermobility has several common neurological and multisystemic manifestations apparent in the literature, although these are not routinely screened for in clinical practice (Castori and Voermans, 2014; Demmler et al., 2019).

If dysregulation is the missing link that ties these two conditions together, a closer look at the brain structures involved in the processes of regulation -- the processes involved in sensitivity to stimuli coming into the nervous system, and returning balance to the body and the brain after arousal or stress ? could shine a light on what these two conditions have in common.

Brain imaging of hypermobile individuals has shown structural differences that indicate autonomic and interoceptive sensitivities, and differences in brain regions linked to emotional regulation (Eccles, et al., 2012). Differences in the anterior cingulate cortex could explain increased autonomic arousal and sensitivity to pain experienced by individuals with hypermobility and ADHD via a more finely tuned sensory representation of internal bodily signals (ibid.). The structural differences observed in the temporal and parietal cortices of the hypermobility group, also seen in autism, can affect proprioceptive awareness (ibid.). Recent studies (Bonamichi-Santos et al., 2018; Senaviratne et al., 2017) have found that a cluster of three ?cousin?conditions often co-occur with the presence of hypermobility, namely hypermobile Ehlers-Danlos Syndrome (hEDS), postural orthostatic tachycardia syndrome (POTS), and mast cell activation syndrome (MCAS). The differences in brain structure found by Eccles et al. (2012) could explain the proprioceptive difficulties and pain sensitivity common in hEDS and the dysregulated autonomic and inflammatory responses that define POTS and MCAS. Hypermobility is usually recognised, assessed, diagnosed and managed by physiotherapists or pain specialists, while ADHD is diagnosed and managed by psychiatrists, and diagnosis in women is extremely delayed for both conditions. There is no natural overlap of these fields in research or practice, except in the bodies and brains of their patients.

The average diagnostic delay for women with hypermobility conditions is 16 years, with ADHD or psychiatric misdiagnosis of 22 years (A.I.S.E.D. et al., 2009). Earlier diagnosis can prevent chronic physical and psychiatric morbidity and improve quality of life for hypermobility and ADHD in isolation, and is even more crucial when these conditions are comorbid. When we know about common comorbidities, we screen for them. This reduces the risks of delayed diagnosis and enables early intervention. If someone has high blood pressure, we also check their cholesterol levels. When we see signs of one condition, we screen for its cousins. While medical textbooks have started to acknowledge that the mind, brain and body are interconnected, our screening protocols remain siloed, and vulnerable patients with multisystemic conditions continue to slip through the cracks. Patients with brain or bodily regulation difficulties have similar brain structures, and would benefit from early screening and management, but these research findings are not currently reflected in clinical practice. Lack of multidisciplinary screening for hypermobility and ADHD results in delayed diagnosis and multimorbidity from a young age, particularly in females; the longer the delay the greater the impact on quality of life (Makovski et al., 2019). To support multisystemic conditions that overlap between specialties, medical education needs to prioritise interdisciplinary training, both in medical school and in continuing

"Dysregulation doesn't happen in silos, and it doesn't stay within the arbitrary lines that themedical system draws between specialties." education. Dysregulation doesn't happen in silos, and it doesn't stay within the arbitrary lines that the medical system draws between specialties. Screening for one type of dysregulation should trigger health professionals to screen for the other types as well. Treatments for the body help the brain regulate, and treatments for the brain help the body regulate. But we can only take advantage of this overlap if we recognise it and screen for it. Looking through a dysregulation lens -- in research, medical education, screening, and clinical referral pathways -- could help disparate disciplines communicate, learn from each other, and improve patient care. Bodies and brains have trouble regulating for many physiological and psychiatric reasons, from ADHD and

hypermobility to chronic pain, attachment trauma, PTSD or concussion. Some of these conditions already have multidisciplinary clinics and proven approaches for managing and improving the capacity for regulation that could be applied to ADHD and hypermobility. First steps in the frontline include updating clinical practice guidelines, interdisciplinary screening, and interdisciplinary management teams, consults, or referral networks. While some researchers have started to link hypermobility and ADHD, more interdisciplinary, longitudinal, health economics, and epidemiological research is required to evaluate the hidden costs of delayed diagnosis and multimorbidity, and the potential impact of improved screening, recognition and collaborative care for dysregulation conditions. Upstream, steps need to be taken to transform the way we learn, share, and update interdisciplinary knowledge. With conditions that involve dysregulation, informed clinicians and researchers learn from multiple specialties, not just their own. We also need to learn from (and update the textbooks to include) the experiences of multisystemic patients, especially when a brain-based treatment helps the body, or a body-based treatment helps the brain. A potential method through which this information could be shared is a reimagined Grand Rounds Q&A, with multisystemic dysregulation patients, clinical follow up and feedback loops that cross disciplines, or multisystemic dysregulation electives and textbooks in medical school. Cultivating interdisciplinary feedback loops and

deliberately sharing knowledge about overlapping treatment outcomes could transform many aspects of research and education, reduce diagnostic delays, and prevent decades of physical disability and psychiatric issues.

and improve long-term physical and mental wellbeing for this vulnerable population.

Ref er ences

Dysregulation ? like neuroscience ? is developmental, multisystemic, and crosses the line between the brain, body, and behavior, affecting the autonomic, attachment, interoceptive, proprioceptive, and inflammatory response systems. We now know that bodies and brains that have trouble with regulation have similar brain structures. If the brain has trouble regulating stress, sleep, behavior or executive function, then we also should check to see if the body is having trouble regulating pain, proprioception, or inflammation. If we recognise one type of dysregulation, it should be standard clinical practice to check for other types and manage them all. Neuroscientists have started to look inside hypermobile brains to reveal fascinating links that connect the dots between the fields of body and brain medicine and reunite a siloed medical system. A growing evidence-base indicates that cross-screening for joint hypermobility and ADHD should be considered as clinical best practice if the signs for either condition are present. Hypermobile bodies and ADHD brains are not separate like the specialties that treat them. Interconnected conditions need interconnected medical support. Working together to recognise and manage these multisystemic conditions early may prevent decades of physical and psychiatric morbidity

A.I.S.E.D., d Associazione Italiana per la Sindrome di Ehlers-Danlos, & The Association Franรงaise des Syndromes d?Ehlers Danlos. (2009). Ehlers-Danlos Syndrome. In Eurordis, The Voice of 12,000 Patients: Experiences and Expectations of Rare Disease Patients on Diagnosis and Care in Europe (pp. 135-142). Eurordis. Baeza-Velasco, C., Sinibaldi, L., & Castori, M. (2018). Attention-deficit/hyperactivity disorder, joint hypermobility-related disorders and pain: expanding body-mind connections to the developmental age. ADHD Attention Deficit and Hyperactivity Disorders, 10(3), 163-175. https://doi.org/10.1007/s12402-018-0252-2 Bonamichi-Santos, R., Yoshimi-Kanamori, K., Giavina-Bianchi, P., & Aun, M. (2018). Association of Postural Tachycardia Syndrome and Ehlers-Danlos Syndrome with Mast Cell Activation Disorders. Immunology and Allergy Clinics of North America, 38(3), 497-504. https://doi.org/10.1016/j.iac.2018.04.004 Castori, M., & Voermans, N.C. (2014). Neurological manifestations of Ehlers-Danlos syndrome(s): A review. Iranian Journal of Neurology, 13(4), 190?208. Cederlรถf, M., Larsson, H., Lichtenstein, P., Almqvist, C., Serlachius, E., & Ludvigsson, J. (2016). Nationwide population-based cohort study of psychiatric disorders in individuals with Ehlers?Danlos syndrome or hypermobility syndrome and their siblings. BMC Psychiatry, 16(1). https://doi.org/10.1186/s12888-016-0922-6 Demmler, J., Atkinson, M., Reinhold, E., Choy, E., Lyons, R., & Brophy, S. (2019). Diagnosed prevalence of Ehlers-Danlos syndrome and hypermobility spectrum disorder in Wales, UK: a national electronic cohort study and case?control comparison. BMJOpen, 9(11), e031365. https://doi.org/10.1136/bmjopen-2019-031365 Do?an, ?., Taner, Y., & Evcik, D. (2011). Benign Joint Hypermobility Syndrome in Patients with Attention Deficit/Hyperactivity Disorders. Turkish Journal of Rheumatology, 26(3), 187-192. https://doi.org/10.5606/tjr.2011.029 Eccles, J., Beacher, F., Gray, M., Jones, C., Minati, L., Harrison, N., & Critchley, H. (2012). Brain structure and joint hypermobility: Relevance to the expression of psychiatric symptoms. British Journal of Psychiatry, 200(6), 508-509. https://doi.org/10.1192/bjp.bp.111.092460 Kumar, B., & Lenert, P. (2017). Joint Hypermobility Syndrome: Recognizing a Commonly Overlooked Cause of Chronic Pain. The American Journal of Medicine, 130(6), 640-647. https://doi.org/10.1016/j.amjmed.2017.02.013 Makovski, T. T., Schmitz, S., Zeegers, M. P., Stranges, S., & Van Den Akker, M. (2019). Multimorbidity and quality of life: Systematic literature review and meta-analysis. Ageing Research Reviews. Ageing Research Reviews. http://doi.org/10.1016/j.arr.2019.04.005 Mu, W., Muriello, M., Clemens, J., Wang, Y., Smith, C., & Tran, P. et al. (2019). Factors affecting quality of life in children and adolescents with hypermobile Ehlers-Danlos syndrome/hypermobility spectrum disorders. American Journal of Medical Genetics Part A, 179(4), 561-569. https://doi.org/10.1002/ajmg.a.61055 Quinn, P., & Madhoo, M. (2014). A Review of Attention-Deficit/Hyperactivity Disorder in Women and Girls. The Primary Care Companion for CNS Disorders. https://doi.org/10.4088/pcc.13r01596 Seneviratne, S., Maitland, A., & Afrin, L. (2017). Mast cell disorders in Ehlers-Danlos syndrome. American Journal of Medical Genetics Part C: Seminars In Medical Genetics, 175(1), 226-236. https://doi.org/10.1002/ajmg.c.31555 Shiari, R., Saeidifard, F., & Zahed, G. (2013). Evaluation of the Prevalence of Joint Laxity in Children with Attention Deficit/Hyperactivity Disorder. Annals of Paediatric Rheumatology, 2(2), 78-80. https://doi.org/10.5455/apr

In side th e Br ain s of M an ?s Best Fr ien d: A Stu dy of Evol u tion ar y Neu r obiol ogy Kelsey H oskin H arvard College, '21 M ajor: H uman Evolutionary Biology Principal I nvestigator: D r. Erin H echt

In 1959, on an unassuming fox fur farm in Russia, two geneticists Dimitri Belyaev and Lyudmila Trut embarked on a research project that transformed our understanding of animal domestication and evolutionary biology entirely. After reading Darwin?s ?On the Variation of Plants and Animals Under Domestication?, the scientists set out to test if the artificial selective pressure for prosocial behavior towards humans was enough to fully domesticate a species. In order to test this hypothesis, they chose the silver fox, Vulpes vulpes, for its close taxonomy to domesticated dogs and easy accessibility on the fur farm. One by one, they behaviorally tested the foxes and artificially selected the individuals they concluded to be the most tolerant, docile, and amicable towards humans, to interbreed. The criteria used was extremely rigorous and as a result, only approximately 10 percent of each generation were chosen to continue breeding. After the 4th generation, all of the aggression had been bred in the foxes and after the 6th generation the fox pups actually began to seek human interaction (Trut et. al., 2009). It was clear that selection for these behavioral traits was indeed sufficient to domesticate the species. This finding was groundbreaking; however, along with this discovery came a surprise. In addition to the dramatic behavioral shift in the fox progeny, there was an astonishingly consistent accumulation of certain unexpected morphological traits. Belyaev noted that these traits were strikingly similar to those of domestic dogs. As the foxes became more and more behaviorally domesticated,

Fig. 1 ?Domesticated? Silver fox exhibiting dog-like traits of domestication syndrome.

they began to exhibit coat depigmentation, floppy ears, curly tails, and the general maintenance of juvenile features (Fig. 1)(Trut et. al., 2009). This host of traits is now recognized as a phenomenon called ?domestication syndrome? and is recognized in most domesticated species. Along with each selection event, some developmental side effect was occurring that altered both the behavior and appearance of the animals. Our lab seeks to further the work of Belyaev and colleagues by investigating the underlying neurological changes that accompany all of the behavioral and morphological changes in these domesticated breeds. In other words, how does brain anatomy and function change in response to selective pressures? We carry out this analysis with a two-fold approach. The first objective of our lab involves the behavioral testing of both domesticated dogs and the Belyaev foxes. As the first known species to undergo

domestication approximately 15,000 years ago, dogs provide an excellent model species to compare to the selectively bred foxes. The idea is that the selective pressures that dogs underwent centuries ago was likely similar to those that Belyaev designed for the foxes. The animals are given similar trials and tasks having to do with their empathy, compatibility, and reliance on humans. The purpose of these tests is to determine behavioral variation between both the domesticated foxes and dogs and between individuals of the same species. Does the level of domestication of the foxes match that of dogs? Do they respond similarly to certain social situations with humans? The trials are filmed and then certain behavioral displays are ?coded? by our team for comparison.

the neurological changes caused by domestication. However, current hypotheses we have for the neuronal changes underlying this behavioral shift involve the activity of the hypothalamus and the pituitary gland. Located deep within the brain, these structures produce neurotransmitters like oxytocin, vasopressin, and serotonin. It is hypothesized that the levels of these hormones could vary greatly between domesticates and their wild counterparts. These highly emotive hormones contribute significantly to social behavior and as such, the distribution of the receptors for these hormones could have drastic effects on the disposition of an animal and human interaction. I am honored to be a part of this lab and we are enthusiastic to continue pursuing the mystery of what makes domesticated animals capable of being man?s best friend.

"In other words, how does brain anatomy and function change in response to selective pressures?"

Our second objective employs structural and functional neuroimaging of the brain matter of both dogs and Belyaev foxes to discover exactly how the brain changes on a neuronal level during the process of domestication. In order to carry out this analysis, we receive left hemispheres of the brains of the Belyaev foxes sent to us from Russia. After sectioning the brain tissue, we use histological methods to analyze the matter using digital microscopy. Analyzing the makeup of these selectively bred fox brains compared to wild fox brains helps us understand the relationship between individual variation in brain organization and the predisposition towards skill learning and adaptation (Hecht, 2020). Our lab is still in its early stages and has a long way to go in order to develop concrete theories to explain

Ref er ences Hecht, E.. (2020 April 23). Personal interview. Trut, L., Oskina, I., & Kharlamova, A. (2009). Animal evolution during domestication: the domesticated fox as a model. BioEssays : news and reviews in molecular, cellular and developmental biology, 31(3), 349?360.

Under standing Two Year Old Childr en?s Poor Per for m ance on a Task of Selective Sustained Attention: Per sever ation and Spatial Resolution Er r or s on the Tr ackI t Task Megan Maxwell Washington University in St. Louis '21 Major: Psychological & Brain Sciences Principal Investigator: Dr. Anna Fisher Research Adviser: Emily Keebler

TrackIt is a task designed to measure selective sustained attention, which undergoes major developmental changes? especially in the preschool years. The task involves visually following a target moving among distractor shapes for a period of about ten seconds until all of the objects disappear. The child must then touch the grid cell last visited by the target. TrackIt has been validated as an age-appropriate measure for three to four year old children; however, recently collected data indicates that two year olds (n=20) performed at chance with a 25% accuracy rate (despite parameter settings being simplified for this age group) while older children performed above this chance level. The goal of this project was to examine whether two year old children?s performance was limited by factors unrelated to attention development, namely perseveration to the same grid location and still developing fine motor skills. In the TrackIt task, the final location of the target shape is randomized and distributed equally among four possible grid cells. Children who exhibit perseveration error might repeatedly select the same grid cell regardless of whether it is correct or incorrect. When a child did so on six or more of ten trials, the child was classified as perseverating based on the binomial test, p=0.01. Perseveration error affected over half of the two year old sample across two testing sessions. Compared to four year olds, the oldest age group that

completed the task with the same parameters, two year olds perseverated more frequently (11 vs 8 children out of 20) in session one, though the relationship between age and responder type was not statistically significant, X2 (1,N=40) = 0.40, p=0.53. In session two, there was a significant association between age and responder type, with two year olds perseverating more frequently than four year olds (12 vs 5 children out of 20), X2 (1, N=40) = 3.68, p=0.05. These results provide suggestive evidence of perseveration as a limiting factor for two year olds. Another possible explanation is that a child might track the target object well throughout the trial but unintentionally click on the wrong grid cell due to underdeveloped fine motor skills. Because of this, a child?s clicking locations are more varied within the cell rather than consistently in the middle. Such errors, termed spatial resolution errors, were operationalized by comparing the precision of two and four year olds? clicks to see how precision relates to less developed motor control. By computing the average distances from the cell center to each click, we observed a significant difference between clicks of the two age groups, suggesting two year olds clicked farther from the center of the cell than four year olds (p<0.01). Our findings indicate that both perseveration and spatial resolution error contribute to two year olds? poor performance on the TrackIt task and highlight features that can be modified to obtain valid measures of sustained attention, which is associated with learning (Mischel et al., 1989). Extending the task to children below age three is important for understanding the dramatic changes associated with the development of attention span during the preschool years. Future directions might involve increasing the number of practice trials as a means of combating perseveration error or increasing grid dimensions to minimize spatial resolution error. Additionally, implementing accessory features such as eye-tracking would help further corroborate our hypotheses regarding spatial resolution error. Ref er ences Mischel, W., Shoda, Y., & Rodriguez, MI. (1989). Delay of gratification in children. Science, 244(4907), 933-938.

M agical Th in k in g an d its Rol e in Con tem por ar y Fan tasy M edia Jonah Goldberg Washingt on Univer sit y in St . Louis '22 Major : Linguist ics Minor : Psychology and Wr it ing Pr incipal I nvest igat or : Dr . Pascal Boyer

Although supernatural beliefs vary widely across cultures, many psychologists and anthropologists hold that all of them? from formal theology to folk notions of luck and even the playground scare of cooties? can be traced back to the same few fundamental principles of ?magical thinking.? Magical thinking describes a variety of subconscious, automatic thought processes that help us rationalize confusing natural phenomena as the work of unseen agents and forces, such as spirits influencing the weather or planetary movement determining the fate of a relationship. Today, humans tend to rely less on these intuitions to explain the world, a transition I find to be marked by the development of the fantasy genre. With the rise of contemporary fantasy, media is created involving supernatural ideas that are meant to be considered untrue, not intended to explain any natural phenomena. I was curious whether this change has made our magical thinking irrelevant, or whether our innate thought patterns might still affect the stories we tell,

even when we explicitly acknowledge that the ideas are fantastical. This article explains key principles of magical thinking and outlines an original experiment suggesting that the magical ideas we find most compelling to read are the ones that fit our evolutionary psychology. In their paper, ?Sympathetic Magical Thinking: The Contagion and Similarity ?Heuristics?,? Paul Rozin and Carol Nemeroff discuss the characteristics and evolutionary origin of the two laws of sympathetic magic, contagion and similarity, supported by their previous experimental work (Rozin and Nemeroff). The law of contagion is responsible for such beliefs as haunted houses and cooties, both ideas that are widespread globally. It states that contact between two objects can cause the essence of one to transfer to the other. In the case of a haunted house, it appears self-evident that a murder contaminated the house, either by binding a malevolent spirit to the property or causing misfortune to befall any future occupants, and we rarely think to question the mechanics of this connection. Likewise, in elementary school, it was obvious how to acquire cooties or protect yourself from them, and we considered this knowledge important, but no child I know can actually say what a cootie is. The power of magical thinking stems from the fact that it is intuitive; we accept it without the higher-level areas of our mind needing to understand it. Rozin and Nemeroff suggest that the law of contagion developed out of adaptations to avoid disease. This gives context to the emphasis on ritual purity and cleanliness in the Abrahamic religions, such as the use of the ritual mikvah bath in Judaism and the sacrament of baptism in Christianity. Early humans did not need to understand the mechanics of bacteria and microbes to avoid infection; they simply needed

a strong intuition that contamination could spread through objects and people. However, as humans cannot shut off this system, we mistakenly worry about contagion of moral and spiritual qualities as well as physical disease. The law of similarity follows an even simpler logic and evolutionary motivation: if it looks like a tiger, it probably is a tiger. Similarity explains practices such as voodoo dolls. It states that two objects that are related in superficial ways also share deeper connections. Given this logic, harming a doll that resembles a particular person and perhaps was made using a lock of their hair should also harm the actual person. Rozin has conducted several experiments showing that this intuition is still prominent in our minds. In one study, students showed poorer accuracy throwing darts at a picture of John F. Kennedy?s face, and were more likely to cringe following throws that hit the center of his face, then they were when throwing at a picture of Hitler or at a blank target (Rozin et al. 1986). In an age before we could create realistic likenesses of others, appearance almost universally did equal reality, and our brains struggle to forget this.

Today, supernatural ideas exist in a separate sphere from our understanding of the world, as evidenced by the word supernatural itself. Fantasy media is now the primary cultural home for magical concepts, and there is no burden of explanation limiting the

ideas we can entertain. Yet magical thinking still seems to drive our stories. Two of the world?s most popular fantasy franchises, Harry Potter and The Lord of the Rings, have plots centered around the law of contagion? Harry can feel Voldemort ?s presence through the scar that Voldemort gave him, and Sauron?s spirit corrupts anyone who gets too close to his ring. Even in a genre meant to showcase impossible worlds, do we still prefer stories that match our evolutionary intuitions? I work in the lab of Dr. Pascal Boyer at Washington University in St. Louis, where we study the effects of evolutionary psychology on cultural transmission and cultural norms. Dr. Boyer supported me in pursuing this question as a personal project under this research umbrella. I compiled lists of magical concepts in two contrasting pieces of fantasy media: Harry Potter, a book series that draws from Western mythologies; and Avatar: The Last Airbender, a TV series that draws from Eastern mythologies (Fandom, Wikipedia). I tagged items as either intuitive (matching contagion or similarity, e.g. ?Voldemort places a piece of his soul into a diary. Years later, when Ginny finds the diary, she is able to use it to communicate with a young memory of Voldemort.?) or unintuitive (not matching magical thinking, e.g. ?An invisibility cloak renders the wearer invisible to others and, according to legend, able to avoid death.?), and created two lists of six items for each story (24 in all). I then shuffled all of these items in a survey, asking 110 participants recruited over Amazon MTurk to rank on two 7-point Likert scales how believable and how interesting they found each idea, as well as to rank their familiarity with each story and with fantasy media as a whole.

After removing 25 participants whose answers indicated that they had not read the survey materials, and running multiple regressions with this data suggesting that familiarity with either story or with fantasy media did not predict believability or interest scores, I found that intuitive items were significantly more believable than unintuitive items (t(1019)=3.16, p=.002). Intuitive and unituitive items were similarly interesting (t(1019)=-1.02, p=.310). This experiment suggests that our magical thinking still plays a role in what ideas we find compelling, even in situations that should be removed from any system of logic. Writers may use this finding to make their magic systems more easy to understand, and readers may consider it when reviewing media and asking why they enjoyed a particular story. A growing body of research is using evolutionary psychology to explain our artistic preferences; however, the field primarily focuses on visual arts and music. Future work should seek to replicate these results and further inquire as to how our environment may have shaped the stories we tell? not just why we tell stories, but how we structure them and which elements enchant and inspire us.

Ref er ences Rozin, Paul, and Carol Nemeroff. ?Sympathetic Magical Thinking: The Contagion and Similarity ?Heuristics.?? Heuristics and Biases, 2015, pp. 201?216., doi:10.1017/cbo9780511808098.013.

?Bending Arts.? Avatar Wiki, avatar.fandom.com/wiki/Bending_arts. ?Magic in Harry Potter.? Wikipedia, Wikimedia Foundation, 23 Nov. 2019, en.wikipedia.org/wiki/Magic_in_Harry_ Potter A Spot of Magic by JD Hancock / CC BY 2.0 https://live.staticflickr.com/7064/7082879 485_f329260feb_b.jpg

partner has the potential to serve as a social resource to decrease threat-related neural activity (Coan, Schaefer, & Davidson, 2006; Maresh, Beckes, & Coan, Grace Anderson1 2013). This effect is Wake Forest Unversity '20 moderated by higher M ajor: Psychology relationship quality (Hughes et Co-Investigators: Sara M edina-DeVilliers2; Nauder Namaky2; al., 2012). The presence of a 2 2 James A. Coan, PhD ; Bethany A. Teachman, PhD familiar individual can make facing a threatening stimulus Emotion regulation (ER) strategies are less antagonizing. important for many health and well-being outcomes, as many Over view of t he Pr esent St udy and psychopathologies are characterized Hypot heses by a decline in ability to regulate The goal of the present study is to emotions (Hughes, Crowell, Uyeji, & evaluate the main and interactive Coan, 2012). Emotions can be effects of SER and ER strategies on regulated both on one?s own through neural response to threat, focusing on ER strategies, including cognitive P300 event-related potential. appraisal and expressive suppression, Electroencephalogram (EEG) and and by the presence of trusted others event-related potential (ERP) data via social emotion regulation (SER). clustered around the parietal regions The current study examines how ER of the brain is an appropriate versus SER affects neural responses to technique to evaluate emotional threat. salience and attentional control due to its high temporal resolution (Schupp, Cognitive reappraisal occurs when an Junghรถfer, Weike, & Hamm, 2003). individual shifts their thinking to P300, a specific ERP, indicates positive change their interpretation of a neural activity around the 150 to 350 scenario (Goldin, McRae, Ramel, & milliseconds timepoint and can be Gross, 2008). This is considered an used to understand the emotional effective strategy for facing negative processing of stimuli, as P300 reflects stimuli and is associated with more attention allocation (Eddy et al., 2015). positive well-being, better control of his/her emotions, and better We hypothesized that individuals will interpersonal functioning (Goldin et al., have less P300 activity in response to 2008; Haga et al., 2009). On the other threat when holding the hand of their hand, expressive suppression involves romantic partners compared to inhibiting behaviors associated with holding the hand of strangers or when emotive expression without alone (Maresh et al., 2013). manipulating the intensity of the Additionally, we hypothesized that emotion. Decreasing expression of individuals who regularly engage in emotion utilizes cognitive resources cognitive reappraisal strategies will and activates the parasympathetic have decreased P300 activity because nervous system, which can be individuals who regularly engage in psychologically exhausting in the this strategy may be better equipped long-term (Goldin et al., 2008). to handle threat. Last, we hypothesized that individuals who are SER utilizes the proximal support of holding the hand of their partner and others. As social baseline theory regularly engage in cognitive explains, humans expect others to reappraisal will have the lowest P300 provide support and to serve as a activity, because these individuals will resource when confronting life benefit from both SER and ER. stressors (Beckes & Coan, 2011). A

Neu r al In dicator s of Social an d Em otion Regu l ation

Met hod Par t icipant s Participants (N = 72, female = 49) were in a romantic relationship for at least 3 months and were recruited from the University of Virginia undergraduate participant pool. The average age was 19.42 years old. Informed consent was collected from both the participant and his/her romantic partner. Mat er ials The Emotion Regulation Questionnaire (ERQ) is composed of 10 questions scored on a scale of 1 = strongly disagree to 7 = strongly agree. High scores indicate more engagement in ER. High scores on the cognitive reappraisal subscale indicate frequent use of cognitive reappraisal, while high scores on the expressive suppression subscale indicate frequent use of expressive suppression (Gross & John, 2003). The ERQ measures ER strategy use over time (Gross & John, 2003). Pr ocedur e Participants and partners completed questionnaires, were fitted to 32-channel EEG caps. Ankle shock electrodes were placed on their ankles (counterbalanced for side) and calibrated to a level of shock (0.2-4.0 milliamps) which was uncomfortable but not painful. Handholding paradigm . Participants completed a handholding paradigm, which is a replicated and reliable measure of threat (Coan et al., 2006; Coan et al., 2017). Participants completed 3 randomized conditions: handholding with their romantic partner, handholding with a stranger, and no handholding (i.e., alone). Participants were separated from their handholding partner by a curtain divider. During each condition, participants were presented with a series of X?s indicating a 20% chance of being shocked (i.e., threat) and O?s indicating no shock (i.e., safe) on a computer screen. Participants were debriefed after the task.

Plan f or St at ist ical Analysis Exploratory analyses were conducted using two hierarchical regression models for each of the 6 central parietal electrodes (CP3, CP4, CPz, P3, P4, and Pz). One model evaluated the interaction effect of social condition (i.e., SER) and cognitive reappraisal on P300 activity, while another evaluated the interaction effect of SER and expressive suppression on P300 activity. Follow-up general linear models were used to evaluate the simple effects when statistically significant interactions were found. Result s Statistically significant results were found at the CPz and P3 electrodes, while non-significant results were found at the Pz, P4, CP3, and CP4 electrodes. See Appendix 1 for a full list of models and results. At the CPz electrode, there was a significant interaction effect between expressive suppression and SER on P300, X2 = 10.32, p = 0.006. Secondary analyses comparing each social condition indicated that the alone condition had the most activity at P300, followed by the stranger and partner conditions, respectively. See Figure 1. There was no significant interaction effect of SER and cognitive reappraisal on P300 activity ( X2 = 3.706, p = .157) or of SER and expressive suppression on P300 activity (X2 = 3.889, p = .143). There was no significant effect of ER strategy on P300 activity, F(3, 66) = .965, p = .415. At the P3 electrode, there was a significant interaction effect between SER and expressive suppression on P300 activity, X2 = 6.60, p = 0.037. Follow-up analyses indicated that individuals who typically use expressive suppression strategies and were in the presence of their partner had the lowest P300 activity. See Figure 2. There was no significant interaction effect of SER and cognitive reappraisal on P300 activity (X2 = 2.522, p = .283) or main effect of ER strategy on P300 activity, F(3, 66) = .494, p = .687.

Discussion While previous findings suggest that individuals who use cognitive reappraisal are more likely to benefit from the presence of a trusted other, current results indicate that individuals who regularly use expressive suppression may benefit the most from SER with a partner (Gross & John, 2003). Cognitive reappraisal has been shown to help couples face stressful scenarios, over and above expressive suppression, while expressive suppression has been shown to increase memory of emotional stimuli, making it less beneficial in the long-term (Richards, Butler, & Gross, 2003). Given SER predicted P300 activity in both the CPz and P3 electrodes, this suggests SER may dampen activity when under threat, which is consistent with previous findings suggesting the presence of a trusted other weakens the threat response (Coan, Schaefer, & Davidson, 2006; Coan et al., 2017). The statistical models used in the current study were exploratory. Each electrode location has its own implications. For example, the CPz electrode has been associated with the Default Mode Network, which is active when individuals ruminate (Jaswal et al., 2019; Gudayol-Ferré et al., 2015). The P3 electrode may be associated with inhibitory processes, explaining significant effects with expressive suppression (Molnár, 1999). Lim it at ions and Fut ur e Dir ect ions Many exploratory analyses were used in the current study. A Bonferroni correction was not used, since the analyses were exploratory. Replication is needed. Future studies should further evaluate how SER interacts with expressive suppression. The presence of a trusted other may act as another form of cognitive reappraisal, benefiting individuals who typically use expressive suppression. Individuals who are high in expressive suppression may also be high in cognitive appraisal and already effective at regulating their

emotions. Many open questions remain about how ER and SER interact to help manage threat.

Tables and Figur es

Figur e 1. Effect of condition on P300 activity at CPz.

Figur e 2. Expressive suppression by condition on P300 activity at P3. Ref er ences Beckes, L., & Coan, J. A. (2011). Social baseline theory: The role of social proximity in emotion and economy of action. Social and Personality Psychology Compass, 5(12), 976-988. Coan, J. A., Beckes, L., Gonzalez, M. Z., Maresh, E. L., Brown, C. L., & Hasselmo, K. (2017). Relationship status and perceived support in the social regulation of neural responses to threat. Social Cognitive and Affective Neuroscience, 12(10), 1574?1583. https://doi.org/10.1093/scan/nsx091 Coan, J. A., Schaefer, H. S., & Davidson, R. J. (2006). Lending a hand: Social regulation of the neural response to threat. Psychological Science, 17(12), 1032?1039. https://doi.org/10.1111/j.1467-9280.2006.01832.x Eddy, M. D., Brunyé, T. T., Tower-Richardi, S., Mahoney, C. R., & Taylor, H. A. (2015). The effect of a brief mindfulness induction on processing of emotional images: An ERP study. Frontiers in Psychology, 6. https://doi.org/10.3389/fpsyg.2015.01391 Goldin, P. R., McRae, K., Ramel, W., & Gross, J. J. (2008). The Neural Bases of Emotion Regulation: Reappraisal and Suppression of Negative Emotion. Biological Psychiatry, 63(6), 577?586. https://doi.org/10.1016/j.biopsych.2007.05.031 Gross, J. J., & John, O. P. (2003). Individual differences in two emotion regulation processes: Implications for affect, relationships, and well-being. Journal of Personality and Social Psychology, 85(2), 348?362. https://doi.org/10.1037/0022-3514.85.2.348 Haga, S. M., Kraft, P., & Corby, E.-K. (2009). Emotion Regulation: Antecedents and Well-Being Outcomes of Cognitive Reappraisal and Expressive Suppression in Cross-Cultural Samples. Journal of Happiness Studies, 10(3), 271?291. https://doi.org/10.1007/s10902-007-9080-3 Hughes, A. E., Crowell, S. E., Uyeji, L., & Coan, J. A. (2012). A developmental neuroscience of borderline pathology: Emotion dysregulation and social baseline theory. Journal of Abnormal Child Psychology, 40(1), 21?33. https://doi.org/10.1007/s10802-011-9555-x Jaswal, S. M., Granados Samayoa, J. A., Kam, J. W. Y., Randles, D., Heine, S. J., & Handy, T. C. (2019). The Influence of Acetaminophen on Task Related Attention. Frontiers in Neuroscience, 13. https://doi.org/10.3389/fnins.2019.00444 Maresh, E. L., Beckes, L., & Coan, J. A. (2013). The social regulation of threat-related attentional disengagement in highly anxious individuals. Frontiers in Human Neuroscience, 7. https://doi.org/10.3389/fnhum.2013.00515 Molnár, M. (1999). The dimensional complexity of the P3 event-related potential: Area-specific and task-dependent features. Clinical Neurophysiology, 110(1), 31?38. https://doi.org/10.1016/S0168-5597(98)00042-2 Richards, J. M., Butler, E. A., & Gross, J. J. (2003). Emotion Regulation in Romantic Relationships: The Cognitive Consequences of Concealing Feelings. Journal of Social and Personal Relationships, 20(5), 599?620. https://doi.org/10.1177/02654075030205002 Schupp, H. T., Junghöfer, M., Weike, A. I., & Hamm, A. O. (2003). Attention and emotion: An ERP analysis of facilitated emotional stimulus processing. Neuroreport, 14(8), 1107?1110. https://doi.org/10.1097/01.wnr.0000075416.59944.49

M or al Fou n dation s in th e Cor on avir u s Pan dem ic Riley Hoffma n Ha r va r d College '23 M a jor : Psychology

oral foundations theory, originally proposed by Jonathan Haidt, provides five moral foundations that humans have evolved to use in order to assess morality (Haidt, 2019). For instance, the care/harm foundation considers our concern for the welfare of others and can trigger prosocial emotions like sympathy. Since proposing the theory, a large part of Haidt ?s work has been exploring how the theory explains differences between political liberals and conservatives. Particularly, he claims that liberals overemphasize the care/harm foundation, whereas conservatives appeal to all five foundations (Haidt, 2019). One paper, by Janis Dickinson, provides further evidence for the theory using the example of climate change. This paper found that indeed, placing a greater weight on compassion and fairness predicted willingness to act on climate change, and that having a greater weight on compassion and fairness predicted being ideologically liberal (Dickinson, 2016).

To test this theory further, I have analyzed numerous news articles from online sources of varying degrees of political bias. I will ask whether news sources that are more liberal will produce articles which rely more heavily on language that acts on the care/harm foundation. An outcome that shows a correlation between political bias and use of care/harm language would provide further evidence for Moral Foundations Theory. On the other hand, a solid finding that more liberal news sources did not use relatively more care/harm language could indicate that there are some other factors at play which determine what language authors chose to use, such as the specific details of the topic of each article.

then selected articles which had headlines pertaining to social distancing during the Coronavirus pandemic. For each news source, I collected its political bias rating from Ad Fontes Media?s website (Ad Fontes Media, 2019). This scale of political bias has the most liberal sources rated with the most negative values and the most conservative sources with the most positive values. In other words, the more negative a source?s ranking, the more liberal the source, according to Ad Fontes Media. I then wrote a Python code in Google Colabs to collect the number of care/harm words used in each article. I determined which words to count from the Moral Foundations Dictionary created by Haidt and colleagues (see appendix).

Met hods I collected 146 articles from 20 different online news sources of ranging political biases. To select the articles, I searched ?social distancing,? ?coronavirus,? or ?COVID? via each news source?s search engine or navigated to its ?Coronavirus? page. I

Result s As shown in Figure 1, the relationship between political bias and number of care/harm words used was a slight negative correlation and statistically significant (r = -0.23, N = 146, p = 4.5 Ă&#x2014; 10? 3).

First, as I chose which articles to include, there could be implicit experimenter bias. Second, I only analyzed 20 news sources and 146 articles. Larger sample sizes could have produced more conclusive result. Finally, my study only used one source of political bias rating.

Fi gu r e 1. above; Fi gu r e 2. below

is highly statistically significant (p = 5.27 Ă&#x2014; 10? 9, N = 146). Discussion

I conducted further analysis to see whether the effect was greater when not considering the degree to which a source is biased liberally or conservatively. The articles from liberal sources (political bias < 0) had an average of 6.518 care/harm words, while the articles from conservative sources (political bias > 0) had an average of 1.708 care/harm words, producing a difference between the two averages of 4.810 care/harm words. As seen in Figure 2, the effect of this comparison between averages

The result, a slight negative correlation between political bias and care/harm usage, is consistent with moral foundations theory, which says that liberals rely on the care/harm foundation more than conservatives do. The statistical significance is great, so this result is not due to chance alone. Though the effect size is small when considering the extent to which a source is biased (Figure 1), it becomes much greater when only considering the two categories of ?liberal? and ?conservative? (Figure 2). This suggests that regarding the utilization of the care/harm foundation, the extent of a source?s political bias does not have as much of an impact as the simple fact of being biased one way or the other. Therefore, the theory that politics is related to use of this particular moral foundation is supported by this study. There are several limitations to this study that could be linked to the low effect size of the correlational result.

In order to improve upon my design, I would suggest a study which is conducted several years in the future, when social distancing is not a current topic. Under these circumstances, a more definitive bank of articles on the topic would exist. The study would pull a much larger array of articles from many more news sources, and the selection of articles would be done by many different experimenters to eliminate experimenter bias. The study would also use various different means of rating political bias. Ref er ences Ad Fontes Media (2019, October). Rankings by Individual News Source. Retrieved March 26, 2020, from https://www.adfontesmedia.com/rankings-byindividual-news-source/?v=402f03a963ba Dickinson JL, McLeod P, Bloomfield R, Allred S (2016). Which Moral Foundations Predict Willingness to Make Lifestyle Changes to Avert Climate Change in the USA? PLoS ONE, 11(10): e0163852. https://doi.org/10.1371/journal.pone.0163852 Haidt, J. (2019, October). Moral Foundations Theory. Moral Foundations Theory. Retrieved March 26, 2020, from https://moralfoundations.org/ COVID-19 Vancouver ?s largest protest by GoToVan / CC BY 2.0 https://live.staticflickr.com/65535/49823981297_4ffb104d0d_b.jpg Appendix Moral Foundations Dictionary: Care/Harm Words (Haidt, 2019) abandon

crush

defensively

exploiting

preserve

securitize

sympathized

abandoned

crushed

defensives

exploits

preserved

securitized

sympathizers

abandons

crushes

destroy

fight

preserves

security

sympathizes

abuse

damage

destroyed

fighter

protect

shelter

sympathizing

abuser

damaged

destroys

fighting

protected

sheltered

sympathy

abuses

damaging

detriment

fights

protects

shelters

violence

amity

damagingly

detriments

guard

ravage

shield

violences

annihilate

defence

empathetic

guarded

ruin

shielded

violent

annihilated

defences

empathetic

guards

ruined

shields

war

annihilates

defend

empathetically harm

ruins

spurn

warl

attack

defended

empathically

harmed

safe

spurned

warring

attacked

defender

empathies

harms

safely

spurns

wars

attacks

defenders

empathise

hurt

safety

stomp

wound

benefit

defending

empathises

hurting

securable

stomped

wounded

brutal

defends

empathising

hurts

securance

stomps

wounds

brutality

defense

empathize

impair

secure

suffer

care

defensed

empathized

impaired

secured

suffered

cared

defenseless

empathizes

impairs

securely

suffers

cares

defenselessness empathizing

kill

securement

sympathetic

caring

defenses

empathy

killed

securements

sympathetically

compassion

defensibility

endanger

killer

secureness

sympathies

compassionate defensible

endangered

killing

secureness

sympathised

cruel

defensibly

endangers

kills

securer

sympathises

cruels

defensing

exploit

peace

secures

sympathising

cruelty

defensive

exploited

peaceful

securing

sympathize

?Ever yth in g W as In ter estin g?: Expl or in g th e M in ds of th e Car ey Lab Audrey Jones Harvard College '22 M ajor: Psychology As a sophomore concentrating in psychology, I was lucky enough to serve as a research assistant in the Carey Lab, which is one of three psychology labs housed within the Harvard Laboratory for Developmental Studies. It operates under the direction of Henry A. Morss, Jr. and Elisabeth W. Morss Professor of Psychology, Susan Carey, who is a recipient of numerous awards, including most recently, the 2020 Atkinson Prize in Psychological and Cognitive Sciences from the National Academy of Sciences. It was a wonderful learning opportunity to work closely with Professor Carey and a team of incredible research fellows, postdocs, and other research assistants to design and conduct studies on developmental and cognitive psychology. Throughout the year, I not only gained a deeper appreciation for psychology as a research field but also learned about the different pathways that Carey Lab members took in arriving at their academic profession. In this interview, I spoke with Professor Carey, Carey Lab Manager Nancy Soja, and Research Fellow Peggy Li about their personal stories, what intrigues them about the field of developmental/cognitive psychology, and advice they have for students interested in psychology research. AJ: Can you t ell m e a lit t le bit about t he hist or y of t he Car ey Lab? What inspir ed it s st ar t and what shaped

it s m ission? Susan Car ey: My first Assistant Professorship was in 1972, so the Carey Lab is very old. At the very beginning, I had only a paid RA and a graduate student, Susan Levine. [The Carey Lab] has evolved in terms of a lab culture. It started just as support for my individual work when I was a beginning Assistant Professor. But you can?t do this work alone -- it ?s like an army -- so you have to put together a lab. As graduate students joined, the lab became a mechanism to support the work of the graduate students. And then as postdocs joined it evolved further to support the work of the postdocs as well. The way a lab supports this work is through organizing, raising money to support the research and the students, and providing the necessary infrastructure. There are just so many parts that are needed to do the research we want to do. AJ: What dr ew you t o psychology and in par t icular t o developm ent al psychology? Peggy Li: I was a computer science major as an undergrad. I think I would have been content being a computer scientist, but a lot of the work was coding data and coding programs, and you'd often have to deal with large programs with functions you didn?t know and would have to figure out. It 's like a black box where you?d have to figure out the input and output,

why there were bugs in the program. But I think a few things happened -- at MIT, as an undergrad, you're required to take some humanities classes, and I took linguistics and loved it because I was introduced to ideas like cognitive universals and language faculty. We were given problem sets using language data and learned about formal ways of characterizing languages, like syntactic structures and phonological rules. And so what you're really doing is trying to figure out what the underlying representations are for the language. I also took some psych classes like sensation and perception where, again, you?re trying to figure out how the mind works. And, I thought, wow, okay, maybe this is what I want to do -- trying to figure out how the mind works, which is actually similar to computer programming, where you?re doing a lot of figuring out what the black box is all about. Later at Penn, my advisor worked on language acquisition. She pushed me in the direction of cross linguistic research -- how you can use differences in language input to get at how our minds are working and learning language and whether or not there are going to be differences in the outcome and learning or not. I was also interested in the research area of language and thought. When I came to Harvard to work with Susan, I looked at number acquisition with Mandarin speakers -- because of the

language differences between Mandarin and English -- and then worked on projects from there. Ultimately, I got into developmental studies through trying to figure out language acquisition. Nancy Soja: When I started as an undergraduate, it felt like everybody knew what their major was going to be, and I felt like I was the only person who had no clue. And not because everything was dull, but because everything was possible. So I was taking whatever classes caught my attention, but I was not taking the intro classes of different fields -- I was taking the higher level classes that were really more about something. So then my sophomore year in the first term, I had signed up for a class called ?Infancy? and it featured different areas of psychology. But it was taught by someone who had been a PhD student with Piaget, so it had a very cognitive and representational and theoretical aspect to the class. And the first meeting of the class, I was like, whoa! And I came out of that first meeting knowing that 's what I wanted to do. Susan Car ey: When I was an undergraduate, I first declared math as a major, but I soon decided that wasn't for me, so I veered to anthropology and did field work in Mexico. I also decided that wasn't for me. Like Nancy, all of these things were interesting to me. The question is, how do you find the match between millions of things that can interest you and also the day-to-day experiences of doing work in that field. So then, I tried biology (this was all before I was a sophomore). As an undergrad at Harvard, you had a yearlong tutorial that was one-on-one with a professor or postdoc, and I had

a postdoc as my tutor who worked on biological clocks. I helped him with his experiments, and at that point they didn't have any idea what the mechanisms underlying the obvious animal capacity to tell time were. But what he saw was that what I was really interested in how they knew that the animals knew how to tell time. He had me read all of the ethological literature of the day. But at the end of this yearlong tutorial, he said to me, you know, you could do this kind of work within biology (ethology), but the future of biology is molecular biology. And there is a new field that 's emerging just now -- it 's called cognitive studies. And the

Image: child engaging in various developmental exercises.

leaders of the field at that time were all at Harvard: Jerome Bruner, George Miller, and Noam Chomsky. My tutor said, I really recommend that you take a course with them because it 's my intuition that the deeper work in the issues that you're interested in are going to be there, not in biology. And so I did. As a junior, I took an introductory course with George Miller and Jerry Bruner. And BĂ¤rbel Inhelder, a collaborator of Piaget, gives a lecture in this course, in which she demonstrates non-conservation. She gets a five year old who somehow isn't shy in front of 300 students, going through and failing liquid

conservation tasks. So I say to my section leader, that was really fascinating, but surely, he's just not understanding the question. You give me 20 minutes with him, and I can make the question clear. She said, well, it happens that there's work going on on this. I can get you some five year olds, and you can see whether in 20 minutes you can get them to see what the question is. So then I was hooked for my major. I ended up working in George Miller 's lab and Jerry Bruner ?s lab and did an undergraduate thesis with George Miller and Peter Wason. But even then I thought, this isn?t what I'm going to do -- I want to do something of more practical importance to the world. So I went off and worked with political refugees in Africa. And then I went to do a MA in African history in London, and that happened to be where Peter Wason was. So I went to Peter Wason?s lab meetings just because I knew him and you know, everything was interesting. And that 's when I figured out -- actually, this [cognitive studies] is what I wanted to do. AJ: Why do you t hink developm ent al psychology is an im por t ant f ield t o st udy? Susan Car ey: It 's been understood since the time of the ancient Greeks that you do not have a theory of mind if, at least in principle, you can't account for how it arises. It 's just central to the issues of understanding the human mind because the adult human mind is so obviously different from babies?. So how is theory of mind acquired, and how do you account for that developmental process? You can be interested in developmental psychology because you want to make a difference in education or clinical applications. But

developmental psychology also seeks to answer one of the fundamental and unsolved problems in cognitive science -- a central, theoretical issue. AJ: What ar e som e of t he m ost int er est ing st udies t o have com e out of t he Car ey Lab? And what is your per sonal f avor it e st udy? Peggy Li: Well, interesting is different than favorite. I think the most interesting studies are the ones where you didn't predict such a thing would happen, even in hindsight. There are lots of those in developmental psychology, where you?re like ?What? The kid doesn?t know this?? Susan Car ey: Yeah, like when you design a study and you have a hypothesis. And if it comes out this way, you're going to interpret it one way, and if it comes out this way, you?ll interpret it another way, and then it comes out a third way all together and you have to rethink the whole thing. I've worked on a million different things, and I don't have any personal favorites. There isn't a student 's dissertation that I've supervised that I didn't love. Nancy Soja: I also would not be able to answer that question. But some of the things that first come to mind are Fei Xu?s work, Peggy?s work on how you map things on different kinds of axes, and also Sandeep Prasada?s work on object-substance construals. AJ: Do you t hink COVI D-19 will cause t he Car ey Lab t o m ake per m anent changes in t he way st udies ar e conduct ed? Nancy Soja: Yeah, actually in a good way. Because being able to do online studies is a good thing for us anyway -- not instead of in-lab studies, but in

addition to in-lab studies. That 's a good thing. And it 's a big deal to set it up, so without the impetus of not being able to do in-lab studies, we might not have gotten to doing online studies. Now, because of [COVID-19], we will have online studies figured out, and our protocol will change to cover this. So, we all do expect if this goes well, that when we're back on campus, we will continue this as one of the ways we run studies. AJ: What ar e som e qualit ies t hat you look f or when hir ing an undergraduat e r esear ch assist ant (RA)? Nancy Soja: For the RAs that I hire for the school year, the single thing that I'm looking for the most when I'm interviewing someone is their engagement in the interview -engagement with the stuff that I'm talking about, excitement, and their ability to make connections. And I sometimes hire people who have no psychology background, so I don't mean that when I'm talking about research, they can make connections from an experienced psychology perspective. I am looking for if they can make any connections and that they're jazzed by it and ask follow up questions or make comments because what we do in the lab speaks to them in some way. So that kind of engagement and enthusiasm is the primary thing I'm looking for. But I also want someone who's going to be really industrious and work hard on their own lab work as well as work hard to support others in the lab. For example, if they see I'm doing some task and it 's taking a long time, that they would offer to help -- to help me and to help each other. We try to have a lab where people help each other, so I am looking for a person who is

not going to be competitive about showing that they're the best in the lab -- but someone who's going to work collaboratively and supportively, be curious about the other work that 's going on in the lab, and be invested in helping the other people in the lab. AJ: For an undergraduat e int er est ed in psychology r esear ch, what advice would you give? Susan Car ey: Just start someplace. Get some experience in different labs if you can, or with different people in the same lab. There's no way of knowing whether this is for you without doing it. You have to do it because you have to see -- do you like the repetitiveness of testing kid after kid on the very same procedure, because you must do that early on in your career. And every time I started a new line of work, I would spend a year back in the lab. When I opened an infant lab, I was there for every baby that was tested the first year of that. When I did monkey work, I went down and did it because otherwise I didn't know if I could believe the data. But also that 's where you get intuitions about what 's really going on. Similarly, you have to be interested in learning how to analyze data and learning why the analyses need to be done right and how they support the inferences you make from data. The products of all intellectual work are really, really interesting. And I think you can even get a sense of what the basis of the arguments are, but you cannot get a sense about what the day-to-day process is and how that matches up with what you like and don't like -- so you really have to do it enough in order to decide that for yourself. I m age Ref er ence https://upload.wikimedia.org/wikipedia/commons/6/69/%D8%B1%D9%88%D8%A7% D9%86%D8%B4%D9%86%D8%A7%D8%B3%DB%8C_%D8%B1%D8%B4%D8%AF _%DA%A9%D9%88%D8%AF%DA%A9_-_%D8%AF%D8%AE%D8%AA%D8%B1_%D 8%A8%DA%86%D9%87_Developmental_psychology_15.jpg

I m pli ca t i ons of COVI D-19 a nd Technology on Educa t i on: An I nt er vi ew wi t h Cogni t i ve Psychologi st Da ni el Wi lli ngha m Serena Chmelar University of Virginia '22 Major: Psychology Daniel Willingham is a cognitive psychologist and professor at the University of Virginia. He graduated with a B.A. in psychology from Duke University in 1983 and then went on to get his Ph.D. from Harvard University in 1990. Initially, Willingham?s research solely involved the neural basis for learning and memory. However, in 2000, he switched paths and began conducting research on education and how cognitive psychology can improve it. He is very well known in the field of educational research and has published several books, including Why Don?t Students Like School?, When Can You Trust the Experts?, and Raising Kids Who Read. In 2017, Willingham was also appointed by President Barack Obama to serve as a Member of the National Board for Education Sciences. It is safe to say that Daniel Willingham is very well known in the field of psychology, but he also has a large impact on his closer community in Charlottesville at the University of Virginia. He is regarded as one of the best professors by many students and is very well known for his

engaging lectures. Further, he chooses to donate all proceeds from the textbook he wrote, Cognition: The Thinking Animal, to local Charlottesville charities, which he allows the students of his lecture to choose at the beginning of the semester. In this interview, I had the privilege of speaking to Professor Willingham about his personal path in psychology, how he got to where he is today, advice for undergraduates studying psychology and his opinion on how COVID-19 is changing education. Q: Starting off, how did you initially decide you wanted to study Psychology? Willingham : Both of my parents were psychologists. My father was a psychometrician, and my mother was a counselor. My uncle was actually an experimental psychologist as well. So, to be honest I was actually interested in not being a psychologist because everybody in my family was. Finally, in my sophomore year of college, I took Intro to Psychology and then I was just hooked. Following that, I took Intro to Cognition and that was where I got really excited and knew what I wanted to do.

Q: What were your favorite opportunities studying psychology as an undergraduate? What advice would you give undergraduate students in terms of what they should get involved with? Willingham : Far and away the part that was most exciting for me was doing an undergraduate thesis, more generally, just getting involved in research. You spend so much time as an undergraduate just sitting in a big lecture hall with 349 of your closest friends listening to what scientists have learned, what other people have figured out. And that ?s exciting and fun, but then actually being a part of the process is what I really valued. Q: What is your most proud accomplishment in your career? What was the biggest challenge you were faced with? Willingham : It ?s hard to say because there have been a number of career moments that have been a big deal for me. One certainly was being published in Psychological Review, because that ?s a theoretical journal and I worked very hard on that paper and on the theory it reported. So that definitely felt like a capstone of a lot of work. Another thing that I?ll add to my proud moments is when psychologists that I really revered indicated that they liked some work I had done. I was at a meeting fairly early in my career and there was a neuroanatomist

at Yale named Patricia Goldman-Rakic and I was giving a talk and saw her in the audience and immediately got very nervous. After my talk, she motioned to me to come talk to her and she basically started grilling me, but in a nice way, showing me that she was actually interested. In terms of the biggest challenge, I think, it ?s going to sound stupid but science is really hard. You?re working on problems that so many people before you have worked on so it 's pretty daunting to think ?I?m gonna succeed,? when all these people before you had trouble figuring out some aspect of behavior. But that 's what made that theoretical paper such a proud moment. Q: How did you get involved with studying education? Willingham : It was very much by accident and it was very much because of University of Virginia connections. E.D. Hirsch, who is retired now from UVA but is very prominent in education, asked to talk with me in 1995, right after I initially came to UVA because he wanted to talk with a cognitive psychologist about education and learning in preparation for a book he was writing. He and I met several times to talk about cognitive psychology and because of that, in 2000 or 2001, he invited me to give a talk to about 500 teachers who were affiliated with his non-profit. I said, ?I don?t know

anything about classrooms or education,? and he said ?No, we get that, we just think it would be interesting for these teachers to hear from a cognitive psychologist.? Rashly, I said yes, and then six months later about two weeks before the talk, I thought, ?What in the world am I going to tell a bunch of teachers about memory, or attention or anything else that they don?t already know?? I got very anxious for the talk, actually about half an hour before the talk I literally told my wife [who is a teacher], ?Don?t come,? because I was so nervous. But I ended up just selecting a bunch of topics from my Intro to Cognition class that seemed to be kind of related to education. To my astonishment, the teachers a) didn?t know most of this content, and b) were very interested. So, that really motivated me. In the audience of that talk was the editor of American Educator magazine, which is published by one of the two large teachers unions and this magazine goes to about a million teachers every quarter. She told me I should write for American Educator, so I started writing what became a regular column called ?Ask the Cognitive Psychologist.? So, that 's how I got involved in education and then by 2007, I just started doing this work full time. Q: In your book, Why Students Don?t Like School, you list many reasons why school is so

unlikeable for many children. What do you think the main underlying problem is in the education system that causes all these problems? Willingham : I do think a lot of it is the fact that you have one too many instructions. A teacher can?t fine tune a student 's experiences to where they are. Curiosity is very fragile in children. If the work that you're trying to entice someone to do seems too difficult or too easy, it 's just not interesting. So, with 28 or so students in the class, all with various levels of preparation, it can only be at the perfect ?just right ? level for a fraction of them. Q: Is there any country that 's ?doing it right ? in terms of education? If not, what is ?right ?? Willingham : That ?s a very complicated question because what might look ideal to us in America, the people in other countries or cultures might say it 's not ideal at all. Part of the reason for that is that education is so saturated in goals, so you can?t just think about whether a system is ?good,? you have to actually define what ?good? is, and even then there's no right answer. Q: How do you think this time of remote learning is changing the education system? Do you think it ?s making people realize certain flaws? Willingham : We don?t have any systematic data on this, so I sort

"... education is so satur ated in goa ls, so you ca n?t just think a bout whether a system is ?good,? you have to a ctua lly define what ?good? is, a nd even then ther e's no r ight a nswer ." -Da niel W illingha m on a 'good' education system

of hear stories and see what my own daughters are experiencing (which is very different for both of them). I think what separates it the most is the extent to which the teachers saw this coming and prepared for it. There?s a lot of chatter on social media about what this is going to mean, but I think one of the things that is most apparent to me is that thinking about this time as an indication of what distant schooling can possibly be is a real mistake. This is not a big experiment in distant learning or homeschooling; this is an emergency measure. We are doing what we have to do as best as we

can under emergency circumstances. I think one of the most interesting things is going to be to see whether or not people now are really soured on the idea of remote learning in the future. Q: As technology becomes increasingly important for education, how do you think we?re going to need to adapt, especially for K-12?

Willingham : What I?ve seen, and again this is mostly anecdotal, the repeated experience seems to be that districts get excited about technology, and not for any reason that ?s super thought through. A lot of time, it ?s some feeling that if they don't engage with technology, we?re falling behind. It feels like you?re not adequately preparing kids if you don?t teach them to engage with technology. But the truth is, the way kids are interacting with technology in most districts is extremely shallow, and it ?s not really enriching their education. In other words, they're not learning coding, or anything much more

sophisticated than using apps. That ?s very useful if the kids are not able to access technology at home because in that case, they absolutely do need that experience with technology. But then everything else about education is about delivering content, and giving kids practice and experience in math, or in history etc. What we?ve found over the last 10-15 years is that there is enormous variation in how well various technological programs actually provide instruction. That sounds like a trivial conclusion, it sounds like you?re just saying ?Some of the apps are good, some terrible,? but the truth is 10 or 15 years ago, it was sort of being presented as if all the applications were going to be good. It was presented that technology would be the way to get around the fact that all kids come in with a different level of preparation, it would adapt to where the student is and provide the ?just right ? level of instruction. But what we?ve found is that it is actually much harder to do than anybody anticipated, so most programs are sort of middleing in their success. The other thing that people have realized about technology, in general, but especially in the last month or so, is the degree to which school and learning in particular are social enterprises ? that the relationship you have with your teacher and being around your peers actually does matter for most kids.

Descar t es' Er r or Descartes was a famous philosopher, and his thoughts regarding the mind were very dualist, believing our mind and brain to be two individual processes. Antonio Damasio, an American neuroscientist, disagrees. He begins ?Descartes?Error ? by describing the case of Phineas Gage, and then compares it to the similar case of Elliot. These two people suffered damage to their ventro-medial pre-frontal cortex, which then resulted in drastic changes to their ability to make reasonable decisions and behave appropriately. Without going too much further into the details of their cases, the book gathers evidence from these cases and describes human decision making mechanisms to prove his case. One piece of evidence that Damasio describes is the Somatic Marker Hypothesis, which claims that feelings/ emotions usually create ?somatic markers,? or feelings in the body, such as nausea for disgust or a faster heartbeat when anxious, to guide

Athena Capo-Battaglia Harvard College '22 M ajor: Neuroscience

behavior. Patients with lesions like Elliot ?s often lack these somatic markers, which leads to poor decision making, explaining how seemingly

level-headed people can lose their jobs, wives, and become socially inept. He then demonstrates the connection between our brain and mind, offering explanations for how we experience the world. By arguing this connection as inseparable, the author shows how a lesion to the brain can thus very plausibly change our

personality. He also argues that, due to the nature of the two cases, the ventro-medial pre-frontal cortex (vmpfc) plays a role in tying emotional value to situations that then allow us to value certain decisions in situations such as at work and in our personal lives (this idea of attributing the vmpfc as having direct influence on emotion is not a consensus reached by experts in the field). Overall, this was an interesting book that had been briefly introduced to me in PSY 14 (Cognitive Neuroscience), but ended up introducing so many new ideas about decision-making and evidence for a more connected mind and brain. Although ?Descartes? Error ? was written in 1994, which could expose it to issues of relevance, I do recommend reading this book if you are interested in decision making/ free will; I myself have bookmarked some interesting pages to look into in the future. I m age Ref er ence Image by ElisaRiva / Pixabay License//c https:dn.pixabay.com/photo/2017/02/13/08/54/brain-2062048 _960_720.jpg

Sp i r i t ed Aw ay Ju stin W on g H ar var d College '22 M ajor : N eur oscience and Philosophy I. The new treatment took a long time. It was a lot of listening to the doctor explain in dry technical terms and signing documents? ?There is a possibility for significant behavioral changes due to changes in emotions and affect, which may manifest in various forms? ? Trust me, that was not my priority when I couldn?t even sleep during the night and function normally during the day. When you are going through the day on an hour of sleep, finishing the day is itself a problem, and any other thing seems insignificant on that scale. After finishing treatment at 5pm, I returned home from the doctor ?s office and was exhausted. I meant to take a nap, but when I woke up, it was 5am. I had expected to wake up before sunset, with the sheets wet, crumpled and entirely untucked from the bed. Ever since the trauma and the nightmares, that had been the case. But tonight, there was no twisting and turning on the bare mattress. I had managed to sleep. Not only that, I stayed unconscious for 12 whole hours. But the difference was more than that. Instead of being jolted awake by nightmares, with the vivid and bitter aftertaste of terror, I was now up with a barren mind. My mind was hazy, like the night outside the window. I could not recall the nightmares that had once caused me to jump out from my bed.

In fact, I couldn?t jump out of my bed at all. When I agreed to do the trial treatment, I was expecting the return of a refreshing buzz. I was promised that I would wake up energized and alive. Now, I couldn?t even remember what that felt like. Yes, I no longer felt the headaches from lack of sleep ? but I could no longer feel my head anymore. I lay on my bed, empty and motionless. After a week of experiencing this, I visited my doctor. She explained that this could be ?part of the documented side-effects that can afflict patients for a long and extended period of time.? ?I am sorry. It is very unfortunate that you are experiencing this. I can recommend you to a psychiatrist for a follow-up. But you did agree to the risks of this trial run, which I had explained clearly and you seemed to understand then. Do you still remember that?? Some time ago ? a long time ago, it seems ? I wanted more than everything to get rid of what was in my head. Last week, the girl in this office was scarred by the traumas and nightmares and thoroughly exhausted. Under her bouncy personality, she was trying her best to keep up and get better, and she was willing to risk everything for that. Now that girl is gone. What did she sign away? Herself? Did she know what she was signing away?

II. It was a nice spring day outside the bustling cafe. White clouds and bright sun hats floated around outside the shop window, but when April walked through the door, she stood out from the blur of colours. Her typical easygoing and springy presence was replaced with jarring, oversaturated colours. Her headband stood out in a discoloured grey. Not a cool, charcoal, kind-of grey, nor a mystic jet grey. It was the kind of grey that stared at you blankly, even as April kept her eyes on the floor. Maybe she had a few bad nights of sleep again. Or her nightmares got worse? She did tell me she was planning to try a novel treatment, did it go wrong? ?Bad night?? As I brought over her regular order, a hot matcha latte with a delicately spun dog on top, and took a quick look at her, she gave the slightest of shrugs ? it was as if the shrug itself was shrugging ? before talking to the lawyer who introduced himself and sat down opposite to her. Her face looked great, actually. In fact, it had been the most rested ever since the nightmares started. The bags under her eyes were gone, her fingers were not frenetically tapping on the table, and her face, for the first time in a very long time, looked rested and calm.

Now, together with the mental scars on her face, her nervous exuberance had dissipated. As she stirred her latte and the foamy dog on the latte dissolved into the green matcha, she was also blending right into the surrounding greenery of the cafe. It took some effort to hear what she said to the lawyer, ?? how could I have ever known? No. How could I imagine what it is like to lose my personality, emotions, memories and everything that added up to who I am?? As the lawyer looked through the stack of papers on the table, she continued, ?Yes, the doctor gave me a contract and I signed it, thinking I would want it. The ?I? then thought differently. The ?I? back then was different. The ?I?did not know how much being me meant to me. But how could she make an informed decision until I experienced it? Can she sign away something if she doesn?t know how important it is?? She let out a barely perceptible sigh and finished the thought, ?Everyday, I live with the consequences of her decision. I am living through the hypothetical ?what-is-it-like? to lose such yourself. I now know how much pain it is causing me.? ?Me, not her.?

Maybe a bit too rested and calm. It was almost dormant. Before, it might have looked tired, but there was boundless energy under it. Behind her nightmare-strained face, she always tried hard to make up with great conversations and spontaneous fun ideas. During the quieter hours of the cafe, she would gossip about the imaginary lives of people who pass by the shop window: ?That clueless guy?s suit is still looking for a matching tie ? this lady on the phone walks and talks with a purpose ? LOOK, a cuuute baby!?

The Harvard Brain Volu m e 1 | Issu e 1 | Spr in g 2020 t h eh ar var dbr ain .com