Volume 4. Issue 3. April 2017
Artificial Intelligence to Predict Autism By Teresa Orbillo
Still Alice: A Realistic Portrayal of Alzheimer’s Disease By Golsa Shafa
Abby, Why Is My Teenager Acting Out Again? By Vanessa Gomes
The Fountain of Youth: Is it Possible? By Carol Chen Cover photo from https://www.pexels.com/photo/baby-s-feet-on-brown-wicker-basket-161534/
1 Image from http://quantumleapalchemy.com/wp-content/uploads/2014/06/bigstock-Colorful-Synapse-System-58099229.jpg
ANN SHENG EDITOR-IN-CHIEF
PRISCILLA CHAN EDITOR-IN-CHIEF
EILEEN LIU LAYOUT EDITOR
KELSEY YANG SUBMISSIONS EDITOR
2016-17 EDITORIAL BOARD
PARANDIS KAZEMI LAYOUT EDITOR
WAN XIAN KOH SUBMISSIONS EDITOR
SAMYUKTHA MOVVA MARKETING DIRECTOR
WAZAIRA KHAN SUBMISSIONS EDITOR
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CLARA HONG WEBMASTER
CONTENTS
Toxic Stress By Sara Farhat
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The Dr. Jekyll and Mr. Hyde of Marijuana
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Abby, Why Is My Teenager Acting Out Again?
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By Sawayra Owais
By Vanessa Gomes
Still Alice: A Realistic Portrayal of Alzheimer’s Disease
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The Fountain of Youth: Is it Possible?
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By Golsa Shafa
By Carol Chen
Testing the Relationship Between Neurogenetics and the Environment in the Development of Resilience: Another Dead End?
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Artificial Intelligence to Predict Autism
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By Luciana Escobar
Image from http://www.brainfacts.org/across-the-lifespan/youth-and-aging/
By Teresa Orbillo
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One cell. All life begins as a single cell. We quickly grow and divide to become this large-headed, small-bodied creature called a baby. As time passes, we continue to mature and gain the cognitive capacity to walk and talk. Soon enough we become the angst-y
Editor’s Note
teenager, just trying to get through school and life. Before you know it, we have become adults, ready to start families of our own. Hopefully as we age, we remember all our experiences and memories shared with friends and family. Let’s go back to that first cell. What did it take for that zygote to develop correctly to form an embryo? And then a fetus? How many steps were there? What were the checkpoints? Once we start t hinking about t he complex process involved in just neurodevelopment, it is amazing that all of us grew up the way we did. Neurodevelopment doesn’t just stop there. Throughout childhood and adulthood, our bodies and brains are constantly changing. On top of that, we are exposed to countless environmental stimuli from stress to drugs. How do these factors impact us? These days, we are also concerned with how we will grow old. What makes some people more likely to develop Alzheimer’s Disease or Parkinson’s Disease? To address these questions, we turn to the field of neurodevelopment and aging. In this issue, we examine the various stages of life and how we are impacted by our own genes and by the external environment. Whether you are interested in early childhood conditions such as autism, or you are curious about the onset of Alzheimer’s, this issue is sure to have something for all ages! Once again, we would like to extend a big thank you to all our contributors for making The Interneuron a success. We would also like to thank our wonderful executive team, without whom, we wouldn’t be able to publish such high-quality work. As always, if you would like to write or draw for our magazine, check out our social media pages or send us an email at: interneuron.utoronto@gmail.com. Thank you for an amazing year! Priscilla and Ann Editors-in-Chief
Contributors Sara Farhat
Golsa Shafa
Sawayra Owais
Carol Chen
Vanessa Gomes
Luciana Escobar Teresa Orbillo
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Art by Parandis Kazemi
TOXIC STRESS By Sara Farhat
Prolonged or excessive activation of the stress response can have damaging effects on learning, behavior and health across life. Also known as toxic stress, it disrupts the development of brain architecture and increases the risk of developing stress-related diseases and cognitive impairment that continues into adulthood. Studies have shown neural circuits that deal with stress are malleable during the fetal and early childhood periods. As such, early experiences can shape how plastic they are, so exposure to toxic stress can affect these developing circuits and hormonal systems that lead to a poorly controlled stress response system as one continues to face threats throughout life. Early exposure to toxic stress makes the stress system either too slow to turn off or overly reactive. This can cause a child to respond impulsively to a situation where a threat does not really exist. Furthermore, the child may remain excessively anxious even when the threat is gone or may misinterpret neutral facial expressions as threats. The hypothalamic pituitary-adrenocortical (HPA) system also plays a role in releasing levels of cortisol when the body is under stress. However, when cortisol is released for prolonged periods of time, it can be destructive by suppressing the immune system and memory systems. Both animal and human studies have also found that prolonged cortisol exposure can change the architecture of regions in the brain important in learning and memory. Others studies have found chronically high levels of cortisol and corticotrophin-releasing hormone, a chemical that regulates the HPA system, can damage parts of the hippocampus which is responsible for both learning and memory. All in all, early exposure to toxic stress disrupts the development of brain architecture as well as cognitive functions well into adulthood. Thus, it is clinically significant to find ways to mitigate the effects childhood toxic stress, allowing individuals to flourish as they become mature adults.
References
 National Scientific Council on the Developing Child. (2005/2014). Excessive Stress Disrupts the Architecture of the Developing Brain: Working Paper 3. Updated Edition. http://www.developingchild.harvard.edu
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Image from http://www.fanpop.com/clubs/inside-out/images/38944870/title/inside-out-fear-photo
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Images from 1: Peter Badenhop by Tino Crisรณ retrived from: http://nu-wproject.blogspot.ca/2011_08_01_archive.html 2: http://epochcreations.com/frankensteins-monster/
The Dr. Jekyll and Mr. Hyde of Marijuana By Sawayra Owais
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Regardless of whether you call it pot, weed, or Mary Jane, it is likely that you have heard of marijuana in the news recently. Justin Trudeau’s government is set to legalize marijuana in the coming year.
Indeed, there are several confounding factors that influence research on cannabis use and schizophrenia, and therefore may explain some of the discrepancies seen in the literature.
As with any controversial issue, there are opposing sides to this proposed legislation.
The toxic chemical that produces the “high” is 9-tetrahydrocannabinol (THC). Wit hout THC,
Adversaries argue that the effects of marijuana have yet to be clearly delineated. Of note, marijuana’s putative relationship with schizophrenia, a mental disorder primarily characterized by cognitive decline, psychosis, and auditory hallucinations, are unknown. For instance, one study proposed that there is no relationship be tween cannabis use and t he development of schizophrenia. Researchers found that relatives of patients with schizophrenia were no more likely to develop schizophrenia themselves if the patient was using cannabis as compared to patients who were not using cannabis (Proal, Fleming, Galvez-Buccollini, & Delisi, 2014). Rather, these researchers argued that genetics were a greater risk factor for the development of schizophrenia. Still, another group found that individuals who used cannabis had nearly a 1.5 times increased risk of developing schizophrenia (Vaucher et al., 2017). Evidently, the literature is still divided as to whether cannabis use is a causative factor in the development of schizophrenia. However, a reductionist perspective, such as this one, is a poor approach to take when determining the etiology of complex mental health disorders.
marijuana does not exert any negative effects. Importantly, there are different levels of THC in different strains of marijuana. Therefore, studies must take into account which strain the participant is using as higher levels of THC is associated with more severe psychosis. Presumably, participants will vary in the strain they abuse, and impact the results accordingly. Now, for every Mr. Hyde, there is a Dr. Jekyll. Indeed, while THC may exert negative effects on the user, there is another ingredient in marijuana, cannabidiol, t hat has been shown t o ha ve neuroprotective effects. In fact, researchers found that cannabidiol not only decreased symptoms of psychosis, but may serve as a treatment for individuals with schizophrenia (Renard, Norris, Rushlow, & Laviolette, 2017). These results have extremely important implications for informing Canadian policy. Policymakers should consider legalizing only certain strains of marijuana, those that have lower levels of THC, to decrease cases of cannabis-induced psychosis. With further research focusing on the relationship between THC and cannabidiol, we come closer to passing legislation that is built on scientific merit and knowledge. Maybe cannabidiol will even get its own special day?
References Proal, A. C., Fleming, J., Galvez-Buccollini, J. A., & Delisi, L. E. (2014). A controlled family study of cannabis users with and without psychosis. Schizophrenia Research, 152(1), 283–288. https://doi.org/10.1016/j.schres.2013.11.014 Renard, J., Norris, C., Rushlow, W., & Laviolette, S. R. (2017). Neuronal and molecular effects of cannabidiol on the mesolimbic dopamine system: Implications for novel schizophrenia treatments. Neuroscience and Biobehavioral Reviews, 75, 157–165. https://doi.org/10.1016/j.neubiorev.2017.02.006 Vaucher, J., Keating, B. J., Lasserre, A. M., Gan, W., Lyall, D. M., Ward, J., … Holmes, M. V. (2017). Cannabis use and risk of schizophrenia: a Mendelian randomization study. Molecular Psychiatry. https://doi.org/10.1038/mp.2016.252
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Abby, Why Is My Teenager Acting Out Again? By Venessa Gomes Adolescents are culturally written off as unruly, irresponsible, foolish, and impulsive, in addition to a slew of synonymous adjectives. Instead of adding labels that depreciate a teenager’s value, it is beneficial to understand their foundations. Why do teenagers behave the way they do, and what benefit can be reaped at the end of the tumultuous period known as adolescence? The human brain was once thought to stop developing significantly in early childhood [1]. Now that we can observe the brain’s structure over the course of a lifetime, there is much evidence supporting another view of the brain’s development timeline. It has been established that grey matter continues to evolve until we reach 25 years old or so. Grey matter is the outer part of the brain and is made up of neuron cell bodies, axons, and protective cells. This part of the brain grows rapidly and abundantly from early childhood until early adolescence. During this period of rapid growth, connections between neurons through which impulses pass, called synapses, increase in number. It is around puberty that these synapses begin to be pruned away [2]. Our brain boasts a ‘use it or lose it’ attitude. Those that we make use of often are retained, but those that are not used deteriorate into oblivion. Teenagers are impulsive [2]. I don’t say that in a condescending way. We take risks, knowing that the cost outweighs the benefit. We drink too much, perform daring tricks, take chances that could and often do end very badly. The question is not one of what, but why we do these things. Recently, there has been a major effort in answering the question of why, of all age groups, adolescents take the most risks. Is it the societal influences, or stereotypes that pressure teenagers to act a certain way? Or is there a biological reason for why we take risks very few adults or children would even consider? We will see that the latter is more significant [3]. While society does play a role in how we behave, adolescent behaviour has not changed over the past centuries despite drastic changes in societal influences. Deep in the structure of the brain resides the limbic system, the part of the brain involved in reward processing. During adolescence, this part of the brain undergoes immense development [1]. Like the rest of the prefrontal cortex, the limbic system incurs a vast overgrowth of synapses, and then these synapses are gradually pruned. When evaluating a cost-benefit relationship, the limbic system is responsible for us asking ‘is the instant reward better than the long-term reward, or vice versa?’, to which our answers might vary. In adolescents, the limbic system is found to be susceptible to the feeling of immediate reward. However, the prefrontal cortex, which is responsible for evaluating these rewards and decision making, lags in development. Until the prefrontal cortex catches up, towards the end of adolescence, the benefits of risk-taking seemingly outweigh rational decision making, so risk-taking becomes more frequent [1,3]. This adolescent stage of life is an important one that allows for creativity and an opportunity for one to learn about their own limits. Given the staggered development that happens in the limbic system and prefrontal cortex, it is only natural that questionable decisions are made. Adolescence creates this critical and optimal period for education, in all facets of life. For that reason, it is critical that we are considerate of the reason behind teenage behaviour instead of it being disregarded as nothing more than a hormonal imbalance.
References 1. Casey, B.J., Jones, R., Hare, T. (2008). The Adolescent Brain. Annals of the New York Academy of Sciences, 1124, 111-126. 2. Romer, D. (2010). Adolescent risk taking, impulsivity, and brain development: implications for prevention. Developmental Psychobiology, 52(3), 263-276. 3. Giedd, J.N., Blumenthal, J., Jeffries, N.O., Castellanos, F.X., Liu, H. et al. (1999). Brain development during childhood and adolescence: a longitudinal MRI study. Nature Neuroscience, 2, 861-863.
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Volume 4. Issue 3. April 2017
Image from https://www.pexels.com/photo/adult-attractive-beautiful-bestfriend-206511/
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Still Alice: A Realistic Portrayal of Alzheimer’s Disease By Golsa Shafa
Numerous movies related to Alzheimer’s disease have been screened over the past twenty years. Namely, “The Notebook” captured the hearts of the audience with the help of its romantic plot. Likewise, “Still Alice”
The realistic portrayal of Alzheimer’s disease is apparent throughout this movie. The title hints at a major aspect of this disease that is often overlooked: simultaneous presence and absence. In a movie
made a lasting impression through a touch of realism that exposed the audience to the debilitating nature of Alzheimer’s disease.
review published in the New York Times, A. O. Scott delves into the “paradoxical situation” and explains how Alzheimer’s disease can make the afflicted
“Still Alice” is the story of a linguistic professor (Alice) at the University of Colombia battling early-onset Alzheimer’s disease. This movie is based on a novel written by Lisa Genova, a neuroscientist. The resulting Hollywood movie also valued scientific accuracy. Juliana Moore has the important role of portraying what Alice experiences as she gets closer to the definitive diagnosis of Alzheimer’s disease. The disease begins with random memor y lapses, eventually leading to cognitive deterioration that deteriorates with time. In this movie, the actors do a fantastic job of conveying the coping strategies of the people around the victim of this neurodegenerative disease. For instance, Alice’s husband (Alec Baldwin) and her daughter (Kristen Stewart) give their full support to Alice. Her daughter still tries her best to communicate despite knowing that her mother is trapped in her own world without the ability to pay attention. This movie also draws our attention to the role of technology in health and disease [1]. For instance, Alice uses her laptop to record messages for herself in order to cope with the unbearable memory lapses.
person absent at times, despite the physical presence [2]. Hence, the title “Still Alice” subconsciously familiarizes the audience with this paradox, and in a subtle way evokes their compassion for the Alice that gets through everyday life, despite missing an important part of her existence: her identity. Alice can still sense her tragic fate despite becoming more and more anxious each time her memory gets worse. Indeed, her brilliant mind is not present anymore and she cannot engage in sim ple conversations with her family. Despite the unfortunate turn of events, her family gives her the support that she needs and deserves. The compassion and patience of those who care for her enable her to be still Alice. To put it briefly, the movies portrays a realistic picture of how Alzheimer’s disease can affect people’s lives. Moreover, this movie is about hope. Contrary to popular belief, that Alzheimer’s patients are not aware of their surroundings, hope is quite tangible for Alice, and likely for other patients. Being emotionally present for Alzheimer’s patients, can alleviate their anxiety and bewilderment. For a novel approach, future movies can focus on the impact of Alzheimer’s disease on the lives of caregivers.
References 1. Kermode, Mark. “Still Alice review – Julianne Moore shines in a performance rich with insight” The Guardian. March 8, 2015. 2. Scott, A. O. Losing Her Bearings in Familiar Places. The New York Times. December 4, 2014 Image from http://saudedomeio.com.br/tag/doenca-de-alzheimer/
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The Fountain of Youth: Is it Possible? by Carol Chen
We’ve all wished at some point in our lives that we could stop time. Luckily, our dreams may indeed come true. A study based on Mackenzee Wittke, an eight-year-old girl from Alberta, reveals that there may be a key to prevent physical aging! Other than her hair and nails, Mackenzie hasn’t grown in years - in fact, she is developmentally (both physically and cognitively) the same as a nine-month-year old infant [1]. And if her case was not bewildering enough, her genetic and chromosomal tests are all perfectly normal. Doctors and specialists are eagerly investigating the genes behind her age-impervious mystery. Dr. Richard Walker, editor-in-chief of the journal Clinical Interventions in Aging, claims that each of us age due to “developmental inertia” [2]. We all have internal genetic programs that push our bodies to sexual maturity, coordinating our bodies’ systems to work together and change in perfect harmony. However, once we reach our physical peak, this developmental inertia does not stop but continues to drive our bodies forward. Our internal systems begin to grow uncoordinated, and age-related diseases such as Alzheimer’s and cancers arise. In Mackenzie, her biological systems are “disorganized” and specific unknown genes have somehow stopped this developmental inertia. Scientists are exploring these age-stopping genes: Dr. Walker and his research team in Florida have sequenced the genomes of 12 girls around the world with similar conditions as Mackenzie. Even though the team found non-hereditary genetic mutations in each girl, the mutations were not in the same gene. However, they did find damage to one of the genes causing developmental inertia. They also suspect that mutations could potentially be on the regulatory genes on the second female X chromosome [3]. Similarly, Eric Schadt, director of the Icahn Institute for Genomics and Multiscale Biology at Mount Sinai hospital in New York, has created a line of stem cells from another girl’s skin using her genome and are using them to grow cells and other building blocks that make up her body [1]. Both scientists hope to unlock the secret to being biologically immortal in our generations’ time. Imagine being able to switch off the right genes at any age and being physically and perfectly the same forever. Science is on its way to discovering the “fountain of youth.” What was once thought of as merely a fantasy may soon become a reality. Would you want to stay forever young? References 1. Goh, S. (2016, November 28). Stopping aging: Researchers study 8-year-old Alberta girl who looks like she’s 2. Retrieved March 25, 2017, from http://globalnews.ca/news/3093760/stopping-aging-researchers-study-8-year-old-alberta-girl-who-looks-like-shes-2/ 2. K., Lanau. (2014). The little girl who may hold the secret to aging. Maclean's. Retrieved May 25, 2017, from http://globalnews.ca/news/3093760/stopping-aging-researchers-study-8-year-old-alberta-girl-who-looks-like-shes-2/ 3. James, S. D. (2013, August 16). 8-Year-Old Never Ages, Could Reveal 'Biological Immortality' Retrieved March 25, 2017, from http://abcnews.go.com/Health/girl-ages-unravel-secret-eternal-youth/story?id=19974247
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Photographer: Ali Sina Ghafoorian Model: Mohammad Ghafoorian
Volume 4. Issue 3. April 2017
Testing the Relationship Between Neurogenetics and the Environment in the Development of Resilience: Another Dead End? By Luciana Escobar
The interaction between genes and the environment in the development of personality characteristics are complex and not fully understood. Whilst much progress has been made in recent years to understand
variants hinders the cognitive advantages related to highly resilient individuals (Brett et al, 2015). This study assumes that the presence of any of these gene variants mentioned earlier leads to less resilience
the neuronal basis for resilience, it is still unclear to what extent these genetic and physical variants result in different personality phenotypes. A recent study
development in the individual, which should lead to poor scores in cognitive tests (Brett et al., 2015).
done by Brett et al. decided to test this complex interaction by studying the neurodevelopment of children raised in poor and positive rearing environments and whether genetic susceptibility could predict their cognitive outcomes (Brett et al. 2015).
The experiment studied children with and without the genetic susceptibility to resilience in both institutionalized and non-institutionalized environment by testing their IQs, working memory and prefrontal cor tex grey matter volume t hroughout t heir development (Brett et al., 2015). The study hypothesized that they would see differential susceptibility. This means that negative rearing environment and genetic susceptibility should lead to worse results, and positive rearing environments and no genetic susceptibility should lead to better results. The study, however, did not find this. Instead, it found a complex mix of theories and non-significant effects. The lack of definitive results in this study highlight the complexity of gene and environment interactions. There is much work to be done in the field of epigenetics to fully understand the complex interactions between genes and the environment.
Resilience has many neuronal and physical markers (Nikolova et al, 2011). Recent data suggests that highly resilient individuals fare better in working memory and cognitive tests, as well as have larger prefrontal cortex volume (Nikolova et al., 2011). There are three gene variants highlighted in this study that are related to resilience development. BDNF rs6265, COMT rs4680, and SIRTI rs3758391(C) gene (Bosse et al, 2012; Witte et al., 2012; Yamakuchi, 2012). These genes hinder the release of BDNF, COMT, and SIRTI respectively, which are vital in neuronal health, development, and metabolism (Park et al., 2011). Thus, the presence of any of these gene
References Brett, Z., Sheridan, M., Humphreys, K., Smyke, A., Gleason, M., Fox, N., Drury, S. (2015). A neurogenetics approach to defining differential susceptibility to institutional care. International Journal of Behavioral Development, 39(2), 150-160. Bosse, K. Maina, F. Birbeck, J. France, M. Roberts, J., Colombo,M. &Matthews, T. (2012) Aberrant striatal dopamine transmitter dynamics in brain-derived neurotrophic factor-deficient mice. Journal of Neurochemistry, 120, 385-395. Nikolova, Y. S., Ferrell, R. E., Manuck, S. B., & Hariri, A. R. (2011). Multilocus genetic profile for dopamine signaling predicts ventral striatum reactivity. Neuropsychopharmacology, 36, 1940– 1947. Park, G., Jeong, J., & Kim, J. (2011). SIRT1 deficiency attenuates MPPþ-induced apoptosis in dopaminergic cells. FEBS Letters, 585, 219–224. Witte, A. V., Kurten, J., Jansen, S., Schirmacher, A., Brand, E., Sommer, J., & Floel, A. (2012). Interaction of BDNF and COMT polymorphisms on paired-associative stimulation-induced cortical plasticity. The Journal of Neuroscience, 32, 4553–4561. Yamakuchi, M. (2012). MicroRNA regulation of SIRT1. Frontiers in Physiology: Vascular Physiology, 3, 1–8.
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Artificial Intelligence to Predict Autism By Teresa Orbillo
Autism Spectrum Disorder (ASD) is a lifelong neurodevelopmental disorder that affects three psychosocial dimensions of human autonomy: social, communication, and behaviour (Thompson, 2013). One out of every 45 children in the US have ASD, and professional diagnosis can occur as early as 2 years old (Craciun et al., 2016). What if it is possible that physicians can learn to detect Autism even earlier? Recently, researchers at the University of North Carolina, Chapel Hill have created an artificial intelligence algorithm that can diagnose ASD in babies as young as 6 months old. The researchers found that babies with ASD compared to typically developing (TD) babies have different brain developmental trajectories that can be shown through brain volume (Burns, 2017). The AI algorithm compares the babies’ brain volumes to effectively predict Autism (children with ASD have a larger total brain volume) (Scudellari, 2017). Additional research is looking into the areas that are enlarged (pallidum, lateral ventricles, and intracranial caudate) and how it may lead to the symptoms of ASD (Turner, Greenspan, & van Erp, 2016). The accuracy of the AI is 81%, which is 31% more precise than the current method of behaviour diagnosis (Burns, 2017). The most common diagnosis assessment used today is the IPA (In-Person assessment) which is a 2-part assessment using both questionnaire and naturalistic observation analysis of the child (Smith, Rozga, Matthews, Oberleitner, & Nazneen, 2017). However, there are detriments to this method of diagnosis including observational bias due to subjective perception, and limited allotted time to view a range of behaviour. Therefore, this AI in accordance with behavioural diagnosis may prove be successful in diagnosing ASD with high validity.
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Volume 4. Issue 3. April 2017
Although ASD currently has no cure, early intervention (EI) deems the most promising treatment in ensuring an autonomous life. Earlier intervention is found to actually increase quality of life and produce better outcomes in social and communication functioning (Adelman, & Kubiszyn, 2017). EIs include: Applied Behaviour Analysis (ABA), Intensive Behavioural Intervention (IBI), Respite programs, and more. These interventions use a variety of methods that are age-appropriate in doctoring adaptive proficiencies, such as: behavioural reinforcement, picture communication systems and social skills. The Karanth & Chandhok (2013) study found that children with ASD who had enrolled in early intervention programs (before the age of 6) were more likely to amalgamate into regular schools. Therefore, integrations of these EIs as early as possible would only prove to be beneficial for these children.
Image from https://encrypted-tbn1.gstatic.com/images?q=tbn:ANd9GcTwaFb8oW3t2b-4b2taXwiE av74FekpetNVxfRLU4jVgV5Y0hU4WQ
In conclusion, this advanced AI is a revolutionary technology that opens new doors in the examination of Autism Spectrum Disorder. Since this new method stems from arithmetic calculation it will be easily accessible to physicians and applicable worldwide. However, the main strain in this method is the implication of placing 6 month old babies in Magnetic Resonance Imaging (MRI) machines to obtain the brain scans, that would have less impending complications. Future technology should focus on less invasive measures that are child-friendly. Scientists are looking into fluorescent carbonaceous nanospheres, an organic dye as an alternative to MRI (Qian, et al., 2014).
References: Adelman, C.R., & Kubiszyn, T. (2017). Factors that affect age of identification of children with an autism spectrum disorder. Journal of Early Intervention 39(1), 18-32. Burns, J. (February 24, 2017). AI predicts autism by comparing babies’ brains. Women@Forbes. Retrieved from: https://www.forbes.com/sites/janetwburns/2017/02/24/ai-predicts-autism-by-comparing-babies-brains/#5ae889ad64a1 Craciun, E.C., Bjorklund, G., Tinkov, A.A., Urbina, M.A., Skalny, A.V., Rad, F., & Dronca, E. Evaluation of whole blood zinc and copper levels in children with autism spectrum disorder. Metabolic Brain Disease 31(4), 887-890. Karanth, P., Chandhok, T.S. (2013). Impact of early intervention on children with autism spectrum disorders as measured by inclusion and retention in mainstream schools. Indian Journal of Pediatrics 80 (11), 911-919. Qian, J Ruan, S., Cao, X., Chen, J., Shen, S., Jiang, X., He, Q., Zhu, J., & Gao, H. (2014). Fluorescent carbonaceous nanospheres as biological probe for noninvasive brain imaging. Journal of Colloid and Interface Science 436, 227-233. Scudellari, M. (February 15, 2017). AI predicts autism from brain scans. IEEE Spectrum. Retrieved from:
http://spectrum.ieee.org/the-human-os/biomedical/imaging/ai-predicts-autism-from-infant-brain-scans
Thompson, T. (2013). Autism research and services for young children: history, progress and challenges. Journal of Applied Research in Intellectual Disabilities, 26(2), 81-107.
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