2012 Student Capstone Journal

Capstone Journal Volume IV 2012

WORCESTER ACADEMY Graduation Projects: Explorations in the Real World

Table of Contents UNDERSTANDING NEUROGENESIS Sally Shepardson, ’12

Pages 4 – 24

The Serial Killer: Media Portrayals, His Origins, and the Legal Implications

by Kaite Zhang Pages 25 – 42

Hunt for the Heretic: The European Witch Hunts as Religious Scapegoating Kiana Nedele, ‘12

Pages 43 – 60

Consider the Jellyfish: Understanding the Process of Ageing and Death

by Angela Niu, ‘12

Pages 61 – 75

UNDERSTANDING NEUROGENESIS Sally Shepardson, ‘12

Introduction Until recently it was believed that neurons were a specific type of cell that did not regenerate. After their initial development, it was believed that the amount of neurons did not increase, but either decreased or remained constant for the majority of an individual’s life. This idea, however, has been refuted by recent studies. Relatively recently, the concept of neurogenesis—the process through which new neurons are formed—has been discovered and discussed. This process, which is now a definite occurrence and not a hypothesis, refutes the idea that neurons are not created during adult life. There are two main regions where neurogenesis occurs in adults: the olfactory bulb and the hippocampus. This paper will primarily deal with the hippocampus because this is the primary location of neurogenesis in the human and mammalian brain.

This paper will look at the two sides of neurogenesis: production and survival. Neurogenesis is a three-step process: progenitors, production and survival. The neurons have to be created through mitosis, which is actually a twostep event itself because there needs to be progenitor chemicals in place for mitosis to occur. The new neurons also need to be selected for survival. The amount of cells produced can affect the rate of neurogenesis, and the rate of survival can affect the rate of neurogenesis. Different hormones, genes, activities, and lifestyles affect either survival or production. This paper will analyze the different environmental and biological aspects of neurogenesis and cell survival, and the pertinence of neurogenesis in the medical field.

The Basics of Neurogenesis

R. Katzman first proposed the “neural reserve theory” to the scientific world.

The theory attempted to explain the observation that with neurodegenerative diseases there seemed to be a gap between functional impairment and the rate of neuron decay. Many scientists, all of whom saw the potential in this phenomenon, further pursued the idea and the theory evolved into a credible fact. The theory stated that neurogenesis, or the production of neurons, continues into the adult years resulting in prolonged cellular plasticity, or the ability to form new neural pathways. The rate of neurogenesis only declines with age; it never ceases, which means that human brains have the ability to create new neural pathways with new neurons all of their lives. This had great implications for cognitive capacity and neural plasticity. The location of this occurrence was soon discovered as well. The main location of neurogenesis in the mammalian brain is the hippocampus, a section of the brain that is typically associated with memory, but is now also associated

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neurogenesis. One area of the hippocampus that has been extensively studied for neurogenesis purposes is the dentate gyrus. This seems to be a particular area of the hippocampus where a great deal of neurogenesis occurs and is often the area targeted in experiments on neurogenesis. The discovery of neurogenesis has great implications on how science views and treats ageing, stroke, dementia, and Alzheimer's. The production of new neurons has implications for how the brain codes for time in memories and may even have behavioral implications. As of now, the majority of the knowledge of the physical effects of neurogenesis remains in hypothesis form.

Though many of the nuances of neurogenesis remain to be discovered or clarified, it is clear that neurogenesis has beneficial properties, especially when it comes to ageing and cognitive ability in the later years of an individual’s life. This prompted scientists to explore whether hormones or lifestyles influence neurogenesis rates. Many different hormones have been studied for their potential role in neurogenesis; these hormones will be discussed in detail later in this paper.

There has also been extensive research on lifestyles and their effect on later life cognitive capacity linked to neurogenesis rates and neural reserve. The predominant outcome of this research is that leading an engaged and active lifestyle and keeping same level of complexity in one’s lifestyle for as long as possible is immensely beneficial to the ageing brain. Individuals who lead active and enriched lifestyles have been shown in some cases to have a higher neural reserve. This serves them well in the later years of their lives.

The concept of neurogenesis has serious medical implications. There have been many discoveries that link neurogenesis properties to tactics for prolonging the coherence of ageing individuals, and regenerative properties have been observed in brains impaired by stroke and Alzheimer’s. The ability for the brain to regenerate neurons after suffering an injury, such as a stroke, or while battling a degenerative disease, such as Alzheimer’s, leaves many researchers and doctors hopeful for a potential cure. If the forces behind neurogenesis could be pinpointed and controlled, then many doors would be opened in the fields of treating cognitive impairments due to age, Alzheimer's and stroke. This paper will discuss the hormones and lifestyle components of neurogenesis, a field that will perhaps prove invaluable in later years (Kempermann, 2008).

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Figure 1: Location of Hippocampus

Figure 2: Location of dentate gyrus

Figure 3: Diagram of a Neuron

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The Role of Learning, Enriched Environments, and Social Interactions

The previous section dealt with the genetics of neurogenesis. This section will deal with the environmental factors of neurogenesis, the very reasons why the genetics of neurogenesis are hard to determine. It has long been stated that neurogenesis is controlled by a variety of environmental factors. The main three factors are learning, environments, and social interactions.

Learning is something we do all of our lives. It is highly beneficial for practical reasons, such as holding a job or self-improvement, but now we know that it increases the survival rate of new neurons. When one learns to associate certain stimuli over time rather than processing random and discontinuous stimuli, newly matured neurons that would otherwise die off are saved and incorporated into new networks. The different types of stimuli reflect the difference between experiencing and learning. The scientific community has long connected the hippocampus with memory, but what they are finding is that the new neurons that are created during a time of learning persist long after the time frame where the hippocampus is responsible for the memories. This suggests that the new neurons in the hippocampus are “saved” by learning. They probably would have died without the stimulation and the brain’s subsequent response to the formation of new memories triggered by learning. There isn’t a great deal of information on how this process occurs. As of now, scientists really only know that new neurons persist if saved by learning, but why or how this occurs remains to be investigated (Leuner et al, 2004).

Another study linked neurogenesis and learning. However, in this study the type of learning was key. Hippocampal dependent learning has been shown to be highly influential on the rate of neurogenesis by increasing the number of surviving cells. There was a dramatic increase in the amount of surviving cells when certain rodents underwent activities that triggered hippocampal learning. When the rodents preformed non-hippocampal learning activities the amount of surviving neurons remained constant. This study supported the idea that learning increased the survival of newly matured neurons, but it also pinpointed the types of learning that increased the survival rate of these new neurons. In mice, special water maze training and trace eye-blink training both involve the hippocampus and increase the amount of newly generated neurons. For the rodents these were slightly more involved and contained different levels of stimuli than the other activities that did not involve the hippocampus, such as delay eye blinking and cue-maze training. The hippocampus dependent activities also involved memory to a higher degree than the non-hippocampus dependent activities. This suggests that not all learning is equal. The brain must be stimulated and involved in a relatively high cognitive activity in order to achieve the positive survival rate. This supports the idea that one should learn and engage in intellectual activities all throughout one’s life. The increased survival rate will have positive impacts later in life and may lessen the effects of cognitive decline seen in old age (Gould et al, 1999).

Engaging and stimulating environments also play a dramatic role in the neurogenesis rate. Being in an environment that is engaging and stimulating, with new objects and places to explore, increases the neurogenesis rate in rodents. While it is well known that what a rat finds engaging and what a human finds engaging are

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very different, the idea that one should get out and explore, to change and redecorate, to do more than stay in the same chair in the same room every day is supported by the finding that enriched environments encourage an increased rate of neurogenesis. This discovery condemns the idea of nursing homes, places where everything remains more or less the same and everything is done for the elderly inhabitants. In order for the elderly to retain the cognitive capacity they have left, they need to be in environments that support increased rates of neurogenesis (Brown et al, 2003). The numbers support this idea. Rodents living in enriched environments have a granular cell layer that is much larger than rodents in a nonenriched environment. There are 15% more granule cell neurons in the dentate gyrus of mice living in engaging environments. Enriched environments allow for stimulation of the brain that leads to an increase of neurons. The positive effects of this are wide and varied, but all will lead to a healthier and happier ageing process (Kempermann et al, 1997).

Social interactions are also highly beneficial to the adult neurogenesis rate. It has been shown that social isolation will actually undo the positive effects of other neurogenesis stimulating activities, such as running (Stranahan et al, 2006). Social isolation can be highly detrimental to the rate of neurogenesis because the lack of stimulus causes a dramatic decrease in cell survival. In the running situation, the new neurons that are created by running are not used if the running is followed by social isolation. Social interactions and the stimuli they create are highly beneficial to the rate of neurogenesis, mostly on the cell survival end of the process. Originally, the reliance on social interactions was thought to be a solely female occurrence (Leasure & Decker, 2009). However, other studies have since proven that the need for social interactions to stimulate and support the neurogenesis rate is something that applies to all genders (Stranahan et al, 2006). While females may be slightly more reliant on social interactions for neurogenesis rate stimulus and cell survival, males have the same basic necessity. The need for social interaction is high and the effects of persistent, constant, and positive social interactions are obvious to many in the scientific world.

The combination of the three environmental factors listed above will lead to a persistently high rate of neurogenesis. This will lead to longer cognitive health and higher cognitive capacity as one ages. It is clear that if these factors are carried throughout one’s life, the benefits will continue. This supports the idea that just because one’s mind starts to fail, one should not be removed from society. In fact, that is when the elderly may need the benefits of society the most.

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Figure 4: Table displaying the effects of trace learning on neuron production

se m ne M ca N 4) or of ei ue

(Leuner et al, 2004).

Figure 3. Trace memory formation persistently enhances the survival of newly born cells in the dentate gyrus. A–C, Acquisition Figure 5: Table displaying the effects of an enriched environment on neuron of the trace eyeblink conditioned response (trace paired) and the unpaired condition. D–F, Total numbers of BrdU-labeled cells in the dentate gyrus of animals 1 d ( D), 30 d ( E), or 60 d ( F) after trace conditioning or unpaired training. Trace conditioning production ageing (Kempermann et al, 1997). increased the number of BrdU-labeled cells when compared with exposure to unpaired stimuli at all survival times. Regardless of training conditions, the number of cells decreased between 1 and 30 d but not thereafter. Bars represent mean % SEM. Significant differences are noted with asterisks.

The number of BrdU-labeled cells in the dentate gyrus did not differ in animals exposed to paired versus unpaired stimuli (t(16) ! "1.6; p ! 0.13) (Fig. 2 B). However, there was a positive correlation (r ! 0.65; p ! 0.03) between the number of BrdU-labeled cells and the percentage of CRs emitted during trace conditioning with paired stimuli (Fig. 2C).

The data presented here stimuli across time rathe uli rescues adult-genera onstrate that once rescu

Physical activity has a significant effect on the rate of neurogenesis in the mammalian brain. However, the location of neurogenesis as a result of physical exercise is restricted solely to the hippocampus. The olfactory bulb, the other location of adult neurogenesis, is entirely unaffected (Brown et al, 2003). The stimulation that occurs when physical exercise is preformed has a positive effect on the hippocampus. The rate of neurogenesis increases, and there is an increased plasticity and dendrite complexity in the brain. Additionally, spine density increases.

The source of this increase has been attributed mainly to the increase of cerebral

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Discussion

The Role of Physical Activity

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blood flow that is a result of physical exercise. Physical exercise also increases cerebral blood volume and blood brain barrier permeability. The cerebral vascular structure changes when physical exercise is performed. The data collected on this phenomenon states that it might have an influential, positive impact on cognitive capacity and neurogenesis. Research indicates that an increase in cerebral blood flow promotes brain function by not only causing the transport of nutrients and oxygen, two things that are key in brain function, but it also increases brain function by transporting neurotrophic factors. These factors support both neural plasticity and neurogenesis. As one ages, the amount of cerebral blood flow declines. This discovery supports the idea that exercise all throughout life may be crucial in the prolonging of sharp cognitive capacity and memory. Neurogenesis, as mentioned before, is a three-part process: progenitors, production and then survival. Some studies have suggested that physical exercise is not active in the survival aspect of neurogenesis (Leasure & Decker, 2009), but in other studies physical exercise has been shown to have a role in cell survival, as well as a role in the rate of neurogenesis. In these studies physical exercise causes neurogenesis, cell survival and also increases the production of hippocampal progenitors, chemicals that are the precursors to hippocampal neuron production and help control the rate of production (Leasure & Decker, 2009; Clark et al, 2009). The controversy on this subject demonstrates the newness of the field of neurogenesis.

The research also shows that a little exercise here and there is not effective.

For physical exercise to have the desired effect on the vascular structure of the brain, consistent exercise is necessary. Consistent exercise for multiple days has been shown to be highly beneficial. However, it was also shown that once physical activity has reached a certain threshold it begins to have a different effect on the brain. This threshold is not linked to the time or duration of the physical activity, but to the intensity; this suggests that there is a minimal level that physical activity needs to reach in order for it to have an effect, whichis not connected to the duration of the activity. Despite this finding, which seemed to pose an alternative for consistent exercise, when it was tested on mice the rate of neurogenesis returned to normal with in one day of the exercise wheel being removed from the cage. This supports the idea that while exercise will be effective at a certain threshold, prolonged and repetitive exercise is the most influential on neurovascular structure because it provides sustained increased rates of neurogenesis.

Additional research suggests that increased cerebral blood flow may not be the neurogenesis increasing mechanism that is affected by exercise. There has been some speculation that the neural pathways formed by the stimulus of exercise and the increase of neurotransmitters, namely serotonin, are what are influential in increased hippocampal neurogenesis. There was even further speculation that it is a combination of these two mechanisms that result in the increased rate of neurogenesis when physical exercise is performed (Van der Borght et al, 2009).

Another study looked at the rate of cell survival for the newly formed neurons. Though there has been some research that seems to support the idea that other factors are required for cell survival of exercise induced neurons (Leasure & Decker, 2009), there has been a fair amount of research that shows that exercise also leads to cell survival. There has been a recent discovery that neurons created

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by exercise are “preferentially recruited� to form new neuron pathways. Running produces neural stimulus as well as neurogenesis, so the brain does form new pathways during the stimulus of running. The new neurons that are formed in the hippocampus during physical exercise are in high demand when these pathways are being formed (Clark et al, 2009). However, the survival of those pathways may be subject to other factors, giving credibility to the theory that cell survival may be contingent on other factors in addition to physical exercise. No matter which way one looks at the relationship between physical exercise and neurogenesis, it certainly is a beneficial activity that one should participate in frequently to lead a long and healthy life.

There are studies done on the influence of the reward aspect of exercise. The brain creates rewarding feelings after running and that takes the form of intracranial self-stimulation. One study tried to determine whether it is this selfstimulation that causes the increased rate of neurogenesis. The findings supported the theory that intracranial self-stimulation through the reward system did enhance the rate of cell proliferation, and it also enhanced the rate of maturation for the newly formed cells. This finding not only advocates for exercise, but voluntary exercise because with voluntary exercise the reward system is triggered. (Takahashi et al, 2009)

The Role of Stress

It has long been stated by the medical community that stress can be detrimental to one’s overall physical health. This seems to be true of neurogenesis as well, for there have been recent, clear breakthroughs that link stress to a significant decrease in the rate neurogenesis. In fact, stress is one of the clearest and most detrimental factors that lead to a decrease both in the rate of neurogenesis and the rate of cell survival. The only other factor that shows an equally strong detrimental effect is age. Stress affects both the rate of cell survival and the rate of cell production. The rate of cell survival is decreased because the brain cannot afford to incorporate neurons into new neurological pathways when under stress, but the main way that neurogenesis is repressed by stress is on the production end.

Stress directly interferes with the rate of neurogenesis, and it attacks both the actual process of neurogenesis and the precursor proteins and chemicals that are needed for neurogenesis to occur. When one is under stress, the level of circulating adrenal steroids is dramatically increased. Adrenal steroids are released directly into the blood stream so they affect the entire body. During stress there is also vasodilatation causing the blood brain barrier to become more permeable. This allows for increased blood flow to the brain. While this occurrence has biological roots in the fact that clear thinking is needed in life or death situations and at times has the ability to increase neurogenesis, as seen in the section on physical exercise, the level of adrenal steroids in the blood during times of stress proves to be a problem. Adrenal steroids directly inhibit proliferation of neurons in the dentate gyrus of the hippocampus. The rate of neurogenesis slows dramatically. This occurs throughout life, starting from birth. No age is exempt from this occurrence.

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Prolonged stress can be very detrimental as the rate of neurogenesis will be perpetually lower than normal. Stress also has negative effects on the precursor proteins and chemicals for neurogenesis. Stresses, and stressful experiences, increase the levels of glucocorticoids, which then stimulate a hippocampal glutamate release. This interferes with the NMDA receptor dependent excitatory pathways. These pathways are directly linked to neurogenesis, and they help trigger the production of new neurons via precursors. However, with stressful experiences, these pathways are either reduced or shut down entirely. This is an indirect way that stress affects the rate of neurogenesis. Stress works at both ends of the production process. It shuts down the ability for the process to start, and it shuts down the process itself. This “one-two punch” is incredibly detrimental to the rate of neurogenesis in the brain and has clear negative effects for future cognitive clarity and capacity, especially in old age (Gould & Tanapat, 1999).

Another study on stress noted that at different ages the effects of stress varied in severity. In this study the effects of stress on the rate of hippocampal neurogenesis was studied in tree shrews at varying ages. The older tree shrews had a much more severe reaction to stress and their level of neurogenesis dropped significantly. It was concluded that as one ages the effects of stress on the hippocampus increases exponentially. However, that does not mean that some ages are exempt from the effects of stress. Even at a relatively young age, stress did have an effect on the hippocampal neurogenesis rate. This goes to show that stress at a young age will have effects later on in life and that continued stress from early in life can be very detrimental in the long term scheme of mental and cognitive health (Simon et al, 2005).

Sleep deprivation can also have similar effects as stress because it triggers similar chemicals in the body. The body responds to sleep deprivation much in the same way that it responds to stress. When one becomes sleep deprived, the levels of glucocorticoids in the body also rise. The effects of glucocorticoids were mentioned earlier. Often sleep deprivation is secondhand to stress, and it is yet unknown if the elevation of glucocorticoids can be linked back to the stress itself or if both stress and sleep deprivation contribute to the increased level of glucocorticoids and the subsequent decline in the rate of neurogenesis. This is a “chicken and egg” problem.

Either way, a reduced stress level and consistent sleep may be an excellent preventive measure against the cognitive decline associated with age (Mirescue et al, 2006).

There are many different kinds of stress. The type that many instantly think of is stress due to work, assignments, lack of sleep, etc. However, social stress is another very real type of stress that can be just as detrimental as the other forms of stress. The effects of social stress have been tested on rodents with the most common procedure being to put an aggressive male into the cage with another, nonaggressive male. The effects of social stress were the same as the other forms of stress: a decline in the rate of neurogenesis. While this has only been tested on rodents, it is not a great leap to assume that similar effects could be seen in human brains. Social stress may take many forms: an unhealthy work or home environment, bullying, etc. While these stressors are sometimes ignored, or

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considered a part of life, they should be addressed, for they pose a threat to not only one’s mental health, but also one’s physical health (Mitra et al, 2006).

Figure 6: Tables displaying the effects of stress (Simon et al, 2005).

Simon et al. / Brain Research 1049 (2005) 244 – 248 245

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The Role of Testosterone

Hormones have a role in the neurogenesis rate. One hormone that is particularly influential in the rate of neurogenesis is testosterone, or androgens, on the broader scope of mammals. Testosterone has long been linked to a general sense of wellbeing, with both women and men experiencing negative repercussions when testosterone levels fall below normal. However, new studies have shown that testosterone has an effect on anxiety, pain perception and cognitive performance.

Androgens have a positive impact on anxiety levels. They significantly lower the anxiety level of an individual. They also increase the cognitive performance of the individual. Individuals with healthy levels of testosterone have clearer and faster Fig. 1. (A) The number of BrdU-labeled cells was significantly reduced thinking patterns than individuals with low levels of testosterone. The effects of after 5 weeks of daily psychosocial stress (n = 18 control; n = 27 stressed

animals). There was no statistical difference in the mean ages of the Control (13.5 months) and Stress (12.7 months) groups. (B) When animals were divided into subgroups according to their ages, an age-dependent vulner10 ability to stress appeared. Results are given as the mean T SEM. Statistics: two-tailed unpaired Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001. (C) After logarithmic transformation of the cell proliferation data, linear regression was used to evaluate the relationship between the log

testosterone are linked to the rate of neurogenesis (Frye & Seliga, 2001). Further studies were done to successfully establish a connection between testosterone and the rate of cell survival. Testosterone, and the components it will eventually break down into, increases the rate of neurogenesis. Testosterone and Dihydrotestosterone both increase the rate of cell survival in the hippocampus.

There is some conflict on the role of estradiol, another breakdown molecule of testosterone. It was originally thought that estradiol had a negative effect on the rate of neurogenesis (Spritzer & Galea, 2007). Soon after, however, other studies emerged stating that it increases the rate of cell proliferation and has a role in cell survival. Most agree that estradiol has a slightly different effect on the rate of neurogenesis because it is involved in both cell proliferation and cell survival (Galea, 2008). The reason behind the initial confusion is the fact that testosterone only is effective in males at a certain time in the formation of the neuron: the ‘axon extension phase.’ Beyond or below that it has a negative effect (Pawluski et al, 2009). By influencing the rate of production and survival, testosterone, or its breakdown molecules, have a clear impact on the neurogenesis rate of an individual.

This explains many of the physical characteristics seen in people with the appropriate amount of testosterone: clear thinking and less anxiety. It also explains the effects on people with low levels of testosterone. Low levels of testosterone throughout life are detrimental to cognitive health in old age. This also explains the cognitive decline associated with “andropause”, when men have sudden decrease in androgen levels and seem to age suddenly (Frye & Seliga, 2001). Perhaps more importantly, the discovery of a hormonal connection to neurogenesis may open doors to the possibility of hormonally controlling the neurogenesis rate of an individual (Spritzer & Galea, 2007).

The Role of Female and Pregnancy Based Hormones Though testosterone affects both males and females alike, there is another set of hormones specific to females. Some of these hormones are present throughout a female’s life, but others are specific to pregnancy. As seen with testosterone, these hormones seem to have a direct correlation with the rate of neurogenesis. The female hormone levels fluctuate throughout a 28-day cycle, making them different from the basic, constant level of hormones that are found in men. Throughout the 28-day cycle, different hormones surge at different times. For females, the surge of progesterone seen in the proestrus phase creates a surge of neurogenesis, and at that time, the rate of neurogenesis in females surpasses that of males. Also, estradiol has a different effect on females than males. It suppresses apoptosis in females, therefore increasing the rate of cell survival and proliferation. It does not have that effect in males. Also, estradiol only enhances cell survival in a certain window of time in males, as mentioned before, where it enhances survival from puberty to death in females. Furthermore, all of the female hormones work together, in different amounts, throughout the menstrual cycle. The different combination of these hormones, and the different amounts of each in the combinations, creates spurts of increased neurogenesis and then the levels return to normal. This is

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another difference between the male and female neurogenesis rates. The femaleâ&#x20AC;&#x2122;s fluctuating hormones create a fluctuating rate of neurogenesis, while the maleâ&#x20AC;&#x2122;s constant levels of hormones create a constant rate of neurogenesis, unless there is an abnormal event that increases or decreases the hormone levels (Galea, 2008; Pawluski et al, 2009).

Pregnancy also has an important role in neurogenesis. Prolactin, a hormone specific to pregnancy, increases the rate of neurogenesis in the female forebrain.

With prolactin-stimulated neurogenesis, the neurons do not always stay in the hippocampus, but will move to the olfactory blub, the location where smells are processed in the brain. This heightens the femaleâ&#x20AC;&#x2122;s sense of smell and may be one of the contributors to the heightened smell sensitivity that is often experienced in pregnancy. Interestingly, if prolactin is introduced artificially to a non-pregnant female, the same effect is seen. This shows that it is prolactin, and not pregnancy itself, that causes this increase in neurogenesis. This occurrence has biological roots.

The role of motherhood is complex and the increase in neurogenesis is one way that the brain is preparing the mother. An increased sense of smell will allow her to be able to identify her offspring and to be on the lookout for predators. The role of prolactin may lead to more studies on artificially increasing the rate of neurogenesis and may be a possible treatment for brain degenerative diseases (Shingo et al, 2003).

The Role of Genetics, Cyclin D2 and TrkB

The role of genetics in the process of neurogenesis has been recently discussed in the scientific community. There is natural variation in the rate of neurogenesis from individual to individual, which led many scientists to believe that there were genes involved. As of now, scientists have located about six genes that they believe to contribute to the neurogenesis characteristics of an individual. What muddies the waters on this subject is the fact that neurogenesis is a rate that is strongly influenced by the environment of the individual. This makes it difficult for scientists to determine whether certain traits are environmentally or genetically controlled. This raises the nature-verses-nurture question. Can some of the genetic factors be trumped by environmental factors and vice versa? Can genetics be manipulated in order to increase neurogenesis rates? Also, are there disorders that may arise out of malformed or missing genes that are influential in neurogenesis?

There are clearly many questions surrounding this relatively new field within the broader field of neurogenesis. Further complicating the research is the fact that neurogenesis is a three part system. There are the progenitors, the actual mitotic process of neurogenesis, and cell survival stage. These three steps may be each controlled by a different set of genes and, as of now, it is very difficult to determine which genes control which steps. The genes that have been identified were mostly found through blind and random tests. As of now, only a few proteins, and therefore genes, have been linked to a specific step (Kempermann et al, 2006).

There are some conditions that may be genetically linked that effect neurogenesis in the mammalian brain. Neurogenesis is a process that involves rapidly dividing cells, so many of the same precursors to cell division that are

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extensively studied with cancer research are also of interest to those in the field of neurogenesis. In the cell cycle, there are proteins that help move it along called cyclins. There are three D cyclins, labeled one through three. A recent study found a connection between cyclin D2 and adult neurogenesis. There is a colligation between D2 formation and genetics because the cyclins are protein based and therefore have to be coded in the individualâ&#x20AC;&#x2122;s genome. If there isnâ&#x20AC;&#x2122;t a gene coding for the production of D2, then it will not exist. This situation has been found and, in mice, the result is a complete lack of neurogenesis. The cause behind this is that D2 helps in the formation of the precursors for neurogenesis, and without the precursors, the actual formation cannot occur. The brain will form in a relatively normal fashion with all of the major parts present, though some parts may be smaller. The real target of this condition is the brain neurons. Though there are three D cyclins, the other two do not have the same effect on neurogenesis as cyclin D2, though all three are found in the hippocampal region. This condition has not been seen in humans, or at least it has not been identified. However, it shines light on the critical role of Cyclin D2 in adult neurogenesis. It also explains why areas of newly formed brain tissue display such high levels of D2. The potential role of cyclin D2 on increasing the rate of neurogenesis has yet to be explored, but could be a future tool in the external manipulation of the rate of neurogenesis in the adult brain (Kowalczyk et al, 2004).

There are other genetic factors that control the survival aspect of neurogenesis. One of them is a gene labeled TrkB. It is also a neurotrophic factor and is active in the formation of new neural pathways in the brain. A study was done on WTmouse the effects of this gene on the rate of cell survival in the hippocampus. Certain mice had this gene, and therefore the factor deleted. Cell survival became compromised because the new neurons were not being preferentially recruited into new neural pathways. Another side effect was anxious behavior from the mice. This suggests that cell survival and the formation of new neural pathways helps regulate mood (Bergami et al, 2008).

Figure 7: The effects of a lack of D2 on the brain (Kowalczyk et al, 2004).

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The Brain and Ageing

There have been many studies that link age with the rate of neurogenesis. All of these studies have found that advanced age correlates with a decrease in the rate of neurogenesis, providing a foundation for some of the cognitive diseases that are seen in the elderly population, such as dementia, and a rationale behind the phenomenon of reduced cognitive capacity and memory that is seen in the elderly population. The decline starts in midlife, and the effects become apparent in old age.

There are many theories that attempt to explain the reasons behind the reduction of neurogenesis with age. One theory is that ageing is linked to elevated levels of circulating corticosterone. This causes an increase in glucocorticoids, something that has already been shown to be detrimental to the rate of neurogenesis in the case of stress. The levels of serotonin, a chemical that decreases in levels in the ageing brain, may also be linked to the decrease of neurogenesis. However, with the elderly population it is well known that a great deal of the environmental factors that support increased rates of neurogenesis tend to disappear; such as physical exercise, enriched environments, learning, and social dominance. The importance of these environmental aspects have been thoroughly documented by scientific researchers and discussed in this paper. Because of the importance in these factors, and the clear lack of many of them in the lives of the elderly population, there remains hope that certain environmental and life style changes may be able to restore the levels of hippocampal neurogenesis in the elderly to young- adult levels (Leuner et al, 2007).

The actual cause behind the reduced rate of neurogenesis does not necessarily have to do with cell survival. The lack of new neurons comes from a decreased rate in the actual process of neurogenesis, and a decrease in the progenitor chemicals and cells needed for neurogenesis to occur. This suggests that the direct cause of the decrease is indeed elevated glucocorticoids levels, because glucocorticoids have a direct effect on the process of neurogenesis itself and the progenitor proteins. The ideas behind the environmental factors may be involved with the management and incorporation of the new neurons that are being produced at the reduced rate and may be more useful in the incorporation of the existing new neurons rather than the production of new neurons (Leuner et al, 2007).

Alzheimer’s

One of the factors that makes the study of the hippocampus and neurogenesis so intriguing to scientists is its possible link to Alzheimer’s. Many scientists hope that further knowledge about the production of new neurons in the brain will shed light on a possible treatment for Alzheimer’s. One study has found a surprising link between Alzheimer’s and neurogenesis. The rate of neurogenesis actually increases as a result of the brain tissue damage that occurs as a result of this disease. Alzheimer’s is a disease in which plaques that contain neuro-toxic chemicals damage brain tissue. This results in cognitive loss and loss of memory.

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Eventually the afflicted individual is left completely disabled and has to be placed in a special care facility. Studies show that there is a link between brain damage and increased rates of hippocampal neurogenesis. The theory is that when brain damage occurs, the rate of neurogenesis increases in an attempt to replace the lost neurons.

This theory was first examined in detail on stroke patients, but the principle applies to any type of brain tissue damage. The same process occurs in Alzheimer’s patients. However, because Alzheimer’s is a disease that progresses, the damage does not stop after trauma occurs, it does not have a finite limit. With Alzheimer’s the damage continues until the death of the afflicted individual. This is possibly the reason why, despite the efforts of the brain to replace the damaged neurons with increased rates of neurogenesis, Alzheimer’s continues to have detrimental effects on the afflicted individual. A point is reached when the damage surpasses the ability for the new neurons to compensate. While this may sound like a failure, it opens many doors to the treatment of Alzheimer’s. There may be a way to artificially increase the rate of neurogenesis throughout the afflicted individual’s life in order to prevent any of the symptoms of Alzheimer’s. While this treatment is still hypothetical and contingent on many variables, it does present itself as a real possibility for the future (Jin et al, 2004).

Stroke A stroke is a blood clot that cuts off blood flow to a certain section of the brain. Often the direct result of this occurrence is the death of the brain matter that was deprived of blood, and therefore oxygen. The individual that suffered the stroke had consequently lost a part of the brain. However, time after time stroke patients have been able to regain a great deal of the skills they lost. The skills were regained due to healing and therapy. This confused many scientists for a while. It was eventually concluded that after time, parts of the brain took over the function of the lost or damaged parts. Now, however, there may be a different explanation: recent studies have found a link between brain damage and an increased rate of neurogenesis. Not only is the rate of neurogenesis increased, but there seems to be a migration pattern for the newly formed neurons. Most of the newly formed neurons migrate towards the ischemic, or damaged, part of the brain. It is almost like the new neurons are replacing the destroyed neurons. The brain has the ability to repair itself, like one would see in the skin cells as they form a scab and then a new skin layer. They then form new neural pathways in the damaged areas. However, these neural pathways are contingent upon environmental factors, which may explain why some skills never return. There have also been findings that show that certain drugs and environmental factors increase the rate of neurogenesis in the ischemic rodent brain, such as drugs used to treat erectile dysfunction. While there is no conclusive evidence of this yet in humans, opportunities have opened in the field of enhancing the ability for the brain to make new neurons after a traumatic brain injury or stroke, and perhaps a combination of drugs and environmental stimuli will prove beneficial to the healing process of a stroke patient (Jin et al, 2006).

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Inflammation

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Inflammation, in many cases, is a detrimental byproduct of an injury or the product of an autoimmune disease. However, studies have found a new reason to be concerned about inflammation: it decreases the rate of neurogenesis in the brain.

Inflammation in the brain is caused by many factors: stroke, brain injury, concussion, Alzheimer’s, or Parkinson’s. All of these occurrences are detrimental to the brain and have negative impacts on memory and cognitive capacity. The inflammation associated with these conditions and traumas have a negative impact on the rate of neurogenesis, according to many studies. The inflammation activates the brain’s own immune cells, the microglia. These specified types of white blood cells produce proinflammatory factors. These factors directly go after new cells, and thus the survival of new neurons dramatically decreases. There is an 80% loss of newly formed dentate neurons when inflammation occurs. Though many brain injuries have been linked to increase rates of neurogenesis, the side effects of the inflammation caused by these brain injuries may offset many of the benefits that * vehicle 35come from the increased rates of neurogenesis. The cells are unable to survive to be days incorporated into new neural networks due to the adverse effects of inflammation.

Iminocycline However, there are many treatments for inflammation. One drug is minocyclin. This drug reduces brain inflammation and restores the rate of neurogenesis by inhibiting the activation of the microglia and has been used in many studies on inflammation.

Also, there are many dietary influences on inflammation. Certain foods have been shown to increase inflammation all over the body. If one has been diagnosed with a condition that causes brain inflammation, a combination of drug treatment and dietary change may be used to restore the proper rate of neurogenesis (Ekdahl et al, 2003).

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ressionof hippocampalneurogenesis. (a and b) The numberof ED1-positive,activated microgliain 5 days (b) after generalized SE(gSE)and partialSE(pSE)with or without minocyclinetreatment. (c ells in the DGat 35 days after gSEwith and without minocyclinetreatment. Arrowheadsdepict in nonstimulatedcontrolsand 35 16 of new neurons in the days after gSEand pSE(28 days SGZ/GCL 7 + 3); in b, n = 13 (4 + 5 + 4) and 14 (5 + 4 + 5); and in e, n = 13 (4 + 5 + 4) and 14 (5 + 4 + 5) mbersfor nonstimulatedcontrols, pSE,and gSEin brackets.Data are number of cells per section. e-treated animals. Hilus,dentate hilus. Scale bar = 50 ,im.

Conclusion The field of neurogenesis is new and still filled with contradicting ideas and studies. However, it is a field that has the potential to be groundbreaking when it comes to the treatment and prevention of many of the aliments, traumas, and diseases that are linked to the brain. The combinations of the environmental, genetic, and hormonal factors involved in neurogenesis both make it complex and variable. But they also allow for multiple paths in the field of manipulating the rate of neurogenesis. There is still a great deal of research to be done on this subject, but what is known now is a promising and hopeful foundation that many cures may be based upon in the future.

Works Cited:

Bergami, M., Roberto Rimondini, Spartaco Santi, Robert Blum, Magdalena GĂśtz, Marco Canossa. Deletion of TrkB in Adult Progenitors Alters Newborn Neuron Integration into Hippocampal Circuits and Increases Anxiety-Like Behavior.

Proceedings of the National Academy of Sciences of the United States of America, Vol. 105, No. 40 (Oct. 7, 2008), pp. 15570-15575

Clark, P. J., Brzezinska, W. J., Puchalski, E. K., Krone, D. A. and Rhodes, J. S. (2009), Functional analysis of neurovascular adaptations to exercise in the dentate gyrus of young adult mice associated with cognitive gain. Hippocampus, 19: 937â&#x20AC;&#x201C;950. doi: 10.1002/hipo.20543

Ekdahl, C. T., Jan-Hendrik Claasen, Sara Bonde, Zaal Kokaia and Olle Lindvall.

Inflammation Is Detrimental for Neurogenesis in Adult Brain. Proceedings of the National Academy of Sciences of the United States of America Vol. 100, No. 23 (Nov. 11, 2003), pp. 13632-13637 Published by: National Academy of Sciences Stable URL: http://www.jstor.org/stable/3148191

Brown, J., Cooper-Kuhn, C.M., Kempermann, G., Van Praag, H., Winkler, J., Gage, F.H., Kuhn, H.G., 2003. Enriched environment and physical activity stimulate hippocampal but not olfactory bulb neurogenesis. Eur. J. Neurosci., 17, 20422046.

Frye, C.A., Seliga, A.M., 2001. Testosterone increases analgesia, anxiolysis, and cognitive performance of male rats. Cogn. Affect. Behav. Neurosci., 1, 371381.

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Galea, L.A.M., 2008. Gonadal hormone modulation of neurogenesis in the dentate gyrus of adult male and female rodents. Brain Res. Rev., 57, 332-341.

Gould, E., Beylin, A., Tanapat, P., Reeves, A., Shors, T.J., 1999. Learning enhances adult neurogenesis in the hippocampal formation. Nat. Neurosci., 2, 26-265.

Gould, E., Tanapat, P., 1999. Stress and hippocampal neurogenesis. Mol. Psychiatry.

46, 1472-1479.

Jin, K., Alyson L. Peel, Xiao Ou Mao, Lin Xie, Barbara A. Cottrell, David C. Henshall and David A. Greenberg. Increased Hippocampal Neurogenesis in Alzheimer's Disease. Proceedings of the National Academy of Sciences of the United States of America Vol. 101, No. 1 (Jan. 6, 2004), pp. 343-347 Published by: National Academy of Sciences Stable URL: http://www.jstor.org/stable/3148422

Jin, K., Wang, X., Xie, L., Mao, X. O., Zhu, W., Wang, Y., Jianfeng Shen, Mao, Y., Surita Banwait and David A. Greenberg. Evidence for Stroke-Induced Neurogenesis in the Human Brain. Proceedings of the National Academy of Sciences of the United States of America Vol. 103, No. 35 (Aug. 29, 2006), pp. 13198-13202 Published by: National Academy of Sciences Stable URL: http://www.jstor.org/stable/30050737

Kempermann, G., Elissa J. Chesler, Lu Lu, Robert W. Williams and Fred H. Gage.

Natural Variation and Genetic Covariance in Adult Hippocampal Neurogenesis. Proceedings of the National Academy of Sciences of the United States of America Vol. 103, No. 3 (Jan. 17, 2006), pp. 780-785 Published by: National Academy of Sciences Stable URL: http://www.jstor.org/stable/30049073

Kempermann, G., Kuhn, H.G., Gage, F.H., 1997. More hippocampal neurons in adult mice living in enriched environment. Nature, 386, 493-495.

Kempermann, G., 2008. The neurogenic reserve hypothesis: what is adult hippocampal neurogenesis good for? Trends Neurosci. 31, 163-169.

Kowalczyk, A., Robert K. Filipkowski, Marcin Rylski, Grzegorz M. Wilczynski, Filip A. Konopacki, Jacek Jaworski, Maria A. Ciemerych, Piotr Sicinski and Leszek Kaczmarek. The Critical Role of Cyclin D2 in Adult Neurogenesis. The Journal of Cell Biology Vol. 167, No. 2 (Oct. 25, 2004), pp. 209-213 Published by: The Rockefeller

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University Press Stable URL: http://www.jstor.org/stable/1622403

Leasure, J.L., Decker, L., 2009. Social isolation prevents exercise-induced proliferation of hippocampal progenitor cells in female rats. Hippocampus.

19, 907-912.

Leuner, B., Mendolia-Loffredo, S., Kozorovitskiy, Y., Samburg, D., Gould, E., Shors, T.J., 2004. Learning enhances the survival of new neurons beyond the time when the hippocampus is required for memory. J. Neurosci., 24, 7477-7481.

Leuner, B., Yevgenia Kozorovitskiy, Charles G. Gross and Elizabeth Gould.

Diminished Adult Neurogenesis in the Marmoset Brain Precedes Old Age. Proceedings of the National Academy of Sciences of the United States of America Vol. 104, No. 43 (Oct. 23, 2007), pp. 17169-17173 Published by: National Academy of Sciences Stable URL: http://www.jstor.org/stable/25450200

Mirescu, C., Peters, J. D., Noiman, L. and Gould, E.. Sleep Deprivation Inhibits Adult Neurogenesis in the Hippocampus by Elevating Glucocorticoids. Proceedings of the National Academy of Sciences of the United States of America Vol. 103, No. 50 (Dec. 12, 2006), pp. 19170-19175 Published by: National Academy of Sciences Stable URL: http://www.jstor.org/stable/30051265

Mitra, R., Sundlass, K., Parker, K.J., Schatzberg, A.F., Lyons D.M., 2006. Social stressrelated behavior affects hippocampal cell proliferation in mice. Physiol.

Behav. 89, 123-127.

Pawluski, J. L., Susanne Brummelte, Cindy K. Barha, Tamara M. Crozier, Liisa A.M. Galea, Effects of steroid hormones on neurogenesis in the hippocampus of the adult female rodent during the estrous cycle, pregnancy, lactation and aging, Frontiers in Neuroendocrinology, Volume 30, Issue 3, August 2009, Pages 343-357, ISSN 00913022, 10.1016/j.yfrne.2009.03.007.

Simon, M., Boldizsa´r C., Fuchs, E., 2005. Age-dependent susceptibility of adult hippocampal cell proliferation to chronic psychosocial stress. Brain Res. 1049, 244-248.

Shingo, T., Gregg, C., Enwere, E., Fujikawa, H., Hassam, R., Geary, C., Cross, J.C., Weiss, S., 2003. Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin. Science, 299, 117-120.

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Spritzer, M.D., Galea, L.A.M., 2007. Testosterone and DHT, but not estradiol, enhance survival of new hippocampal neurons in adult male rats. Dev. Neurobiol., 67, 1321-1333.

Stranahan, A.M., Khalil, D., Gould, E., 2006. Social isolation delays the positive effects of running on adult neurogenesis. Nature Neurosci., 9, 526-533.

Takahashi, T., Zhu, Y., Hata, T., Shimizu-Okabe, C., Suzuki, K., Nakahara, D., 2009.

Intracranial self-stimulation enhances neurogenesis in hippocampus of adult mice and rats. Neuroscience, 158, 402-411.

Van der Borght, K., Kobor-Nyakas, D.E., Klauke, K., Eggen, B. J.L., Nyakas, C., Van der Zee, E. A., Meerlo, P., 2009. Physical exercise leads to rapid adaptations in hippocampal vasculature: temporal dynamics and relationship to cell proliferation and neurogenesis. Hippocampus. 19, 928-936.

http://www.genesmart.com/products/inflammation_nation/20.php?page_id=153

Figure 1: http://www.google.com/imgres?q=hippocampus&hl=en&gbv=2&biw=1232&bih=6 38&tbm=isch&tbnid=85iCuJV59Q4QVM:&imgrefurl=http://www.macalester.edu/p sychology/whathap/UBNRP/ltp04/structure.htm&docid=XBYqNQHMOGBOjM&img url=http://www.macalester.edu/psychology/whathap/UBNRP/ltp04/hippocampu s.jpg&w=725&h=716&ei=yjHT4rDNKfx0gHAhYixDw&zoom=1&iact=rc&dur=530&sig=110469272275042815 147&page=1&tbnh=120&tbnw=122&start=0&ndsp=20&ved=1t:429,r:10,s:0,i:95&t x=57&ty=92

Figure 2: http://www.google.com/imgres?q=dentate+gyrus&hl=en&sa=X&gbv=2&biw=1232 &bih=638&tbm=isch&tbnid=s1TFkop7qCVVmM:&imgrefurl=http://www.psychedu cation.org/mechanism/images/NeurogenesisDetails.htm&docid=ysAcFpxpTSYGm M&imgurl=http://www.psycheducation.org/mechanism/images/Seahor9.gif&w=3 52&h=276&ei=mujHT-zVFYbi0QHgJTcDw&zoom=1&iact=rc&dur=550&sig=110469272275042815147&page=1&tbnh =130&tbnw=166&start=0&ndsp=21&ved=1t:429,r:4,s:0,i:93&tx=134&ty=70

Figure 3: http://www.google.com/imgres?q=neuron&hl=en&biw=1232&bih=638&gbv=2&tb m=isch&tbnid=yq3fWGAwg973GM:&imgrefurl=http://webspace.ship.edu/cgboer/t heneuron.html&docid=BhtVqrZnXJW4QM&imgurl=http://webspace.ship.edu/cgbo er/neuron.gif&w=700&h=500&ei=aejHT72nKOXX0QGdwpnRDw&zoom=1&iact=rc &dur=378&sig=110469272275042815147&page=1&tbnh=123&tbnw=169&start= 0&ndsp=18&ved=1t:429,r:2,s:0,i:143&tx=146&ty=67

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Figure 4: Leuner, B., Mendolia-Loffredo, S., Kozorovitskiy, Y., Samburg, D., Gould, E., Shors, T.J., 2004. Learning enhances the survival of new neurons beyond the time when the hippocampus is required for memory. J. Neurosci., 24, 7477-7481.

Figure 5: Kempermann, G., Kuhn, H.G., Gage, F.H., 1997. More hippocampal neurons in adult mice living in enriched environment. Nature, 386, 493-495.

Figure 6: Simon, M., Boldizsa´r C., Fuchs, E., 2005. Age-dependent susceptibility of adult hippocampal cell proliferation to chronic psychosocial stress. Brain Res. 1049, 244-248.

Figure 7: Kowalczyk, A., Robert K. Filipkowski, Marcin Rylski, Grzegorz M. Wilczynski, Filip A. Konopacki, Jacek Jaworski, Maria A. Ciemerych, Piotr Sicinski and Leszek Kaczmarek. The Critical Role of Cyclin D2 in Adult Neurogenesis. The Journal of Cell Biology Vol. 167, No. 2 (Oct. 25, 2004), pp. 209-213 Published by: The Rockefeller University Press Stable URL: http://www.jstor.org/stable/1622403

Figure 8: Ekdahl, C. T., Jan-Hendrik Claasen, Sara Bonde, Zaal Kokaia and Olle Lindvall.

Inflammation Is Detrimental for Neurogenesis in Adult Brain. Proceedings of the National Academy of Sciences of the United States of America Vol. 100, No. 23 (Nov. 11, 2003), pp. 13632-13637 Published by: National Academy of Sciences Stable URL: http://www.jstor.org/stable/3148191

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The Serial Killer: Media Portrayals, His Origins, and the Legal Implications

by Kaite Zhang PREFACE This essay is divided into the following parts: I. Abstract II. What is a serial killer?

III. Media Portrayal IV. Antisocial Personality Disorder V. Origins a. head trauma b. hormones and genetics c. childhood environment VI. Legal Implications VII. Conclusion VIII. Works Cited I. Abstract “Serial killer.” The term alone summons images of deranged madmen that stalk the night for victims, bringing blissful death only after torturing them with unimaginable cruelty.

Serial killers are “monsters” and “psychos,” inhuman and insane, social constructs created by public fascination in their inexplicability. While individual serial killers are human and complex, deconstructed only by the convergence of multiple scientific fields, the serial killer as a social construct has transformed into a dimensionless being that is defined in singularities perpetuated by media, film, and literature. However, the reductionist nature of media and art, which often pinpoints a single factor behind the creation of a serial killer, fails to capture and convey the complexity of the serial killer. By claiming that there is a definite answer for why a serial killer—fictional or not—became a serial killer, mass media suggests that all serial killers can be so easily explained and reduced into the components of their past or their biology. This is most certainly not the case. Serial killers, like all other human beings, are complex creatures, explained by neither biological science nor social science alone. Only through the confluence of both fields can researchers attempt to understand the serial killer. There is no single, deciding factor in the creation of the serial killer. By examining him through multiple lenses, scientists are able to partially transform him from myth to man and build his profile to aid law enforcement in his capture and prosecution.

Biology and sociology both offer possible sources and indicators of violent personalities.

First, neurologists have associated head traumas to reduced ability in emotion regulation and impulse control, which may compel an individual who has fantasized about killing to live out his fantasies and kill. Second, scientists have connected certain hormones and neurotransmitters to violence. More specifically, the same class of neurotransmitters, catecholamines, that give

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addicts their “high” is connected to pleasure from violence and crime. Also, geneticists have also found that certain genes—particularly the monoamine oxidase A gene—that catabolize catecholamines may cause a predisposition to violence and crime. Finally, sociologists, through a number of case studies, have discovered a correlation between children from abusive or broken homes and criminal activity or delinquency. In an environment where abuse and pain substitutes for love and comfort, it is natural that one may connect the two and revel in sadistic fantasies where love is pain.

All three aforementioned factors are connected to violence and aggression and may possibly be connected to the development of the serial killer. That is, all three have been implicated in the development of antisocial personality disorder, or psychopathy, which seems to be the only thread tying together serial killers, who vary by their preferences and their modes of torture and murder. Mental illness is notably higher amongst serial killers than in the general population, and the majority of serial killers are psychopathic. That is, they suffer from antisocial personality disorder (antisocial personality disorder), the psychiatric diagnosis of a remorseless, amoral individual who understands the difference between right and wrong but does not have the capacity to acknowledge social or moral restrictions or consequences for his actions. APD is the element that separates serial killers from other violent criminals and it is what gives them the ability to kill over and over again. Because sufferers of APD are amoral and often impulsive, they have no guilt after killing and no regard for their own wellbeing and freedom. This suggests that antisocial personality disorder can be directly correlated to a strikingly higher probability of becoming a serial killer. Although having antisocial personality disorder does not doom an individual to a lifetime of murder, the probability is much greater when there is a convergence of APD and one or more of the three factors above. After all, there is no magical formula for “the” serial killer. There are many formulas that use the same four ingredients: genetics, head trauma, childhood environment, and antisocial personality disorder.

If there are more ingredients in the recipe and greater quantities of each ingredient, there is a greater likelihood that the resultant individual will become a serial killer—but that is not a definite outcome.

There are two serious complications of successful research on the serial killer. First, the significant influence of psychopathy on serial killers raises the dilemma of the admissibility of antisocial personality disorder as a mental disease or defect in criminal court. Traditional law and ethics suggest that serial murderers, due to the atrocious nature of their crimes, should be incarcerated for life or even executed. Yet when the majority of killers have a disorder included in the Diagnostic and Statistical Manual of Mental Disorders, the courts and politicians have the responsibility of determining whether a serial killer with antisocial personality disorder can truly be held accountable for his crimes. With this notion that serial killers only kill because of a mental disease or defect, there is another implication: are some serial killers “doomed,” so to speak, to become serial killers? Are they not responsible for their urges to kill, over and over again? Or is it simply this society’s cowardice in the face of true evil that compels us to find a rational scientific, explainable answer, a reason behind such depravity? To attain such an answer, we must examine serial killers through the lens of public opinion, biology, sociology, psychology, and criminal court, as only the confluence of these disciplines can yield a satisfactory theory on why some humans kill other humans, over and over again.

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II. What is a Serial Killer?

Serial killers may seem like recent phenomenon, traceable, perhaps, only as far back as to Jack the Ripper of Victorian England. After all, up until the mid-twentieth century, they were never called “serial killers;” the first documented use of the term was in Merriam Webster’s 1961 Third New International Dictionary (Schechter 6). It was not until 1981 that the term was first published by the media (Schechter 7). Even then, “criminologists have all but ignored multiple murder,” regarding it as “a special case of homicide,” as “a psychiatric phenomenon,” or as “not only rare but also aberrational enough to be unworthy of research attention” (Fox 409). Therefore, it is no surprise that when it comes to serial killers, “speculation outweighs valid and reliable research data” (Scott 2). Research on serial killers is limited not only by restrictions in the attitudes towards serial killers but also by inhibitions in technology and sample size. “The low prevalence of multiple homicides means that current theories will take many years to test” (Scott 2); testing is also limited by the fact that it is “impossible and immoral” to develop a potential serial killer in the lab, release him, and then “study him in his natural environment” (Haringa). The only reliable method for studying serial killers is to take as many case studies as there are available and find the common denominator between the true serial killers.

But what is a true serial killer? What differentiates Jeffrey Dahmer, who killed (and likely ate) a confessed seventeen victims over a fourteen-year span (Schechter 202-203), from a hired assassin? What makes Charles Manson and his followers different from Hitler’s Third Reich (Fox 408)? There is no single answer, as the definition of serial murder is disputed by various authorities. The official FBI Crime Classification Manual states that serial murder is the accumulation “three or more separate events in three or more separate locations with an emotional cooling-off period between homicides,” a definition that seems limited by an arbitrary number (why three?) and jargon (like “cooling-off period”) (Schechter 7). On the other hand, the National Institute of Justice definition is as follows: A series of two or more murders, committed as separate events, usually, but not always, by one offender acting alone. The crimes may occur over a period of time ranging from hours to years. Quite often the motive is psychological, and the offender’s behavior and the physical evidence observed at the crime scenes will reflected sadistic, sexual overtones.

(Schechter 9)

Schechter states that not only does the National Institute of Justice definition exclude professional assassins, who kill as a career rather than for pleasure, and institutionalized killings (such as that of Nazi Germany), this definition quite adequately matches the social construct of a serial killer, imagined by the media and often portrayed as the embodiment of pure evil (Schechter 9).

Now, having separated serial killers from perpetrators of institutionalized murder, scientists and criminologists must also separate serial killers from other individuals who commit multiple murders, of which there are two major categories. One is the mass murderer, who is often described as a “human time bomb,” someone who simply “snaps” one day and attempts to kill as many people as possible, before killing himself (Schechter 10). A subset of the mass murderer is the spree killer, who is essentially a “mobile mass murderer” (Schechter 12). Both the mass murderer and the spree killer are often suicidal, ending their acts by pointing their firearm at themselves or at police.

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Serial killers, however, are more closely related to rapists than mass murderers, as “serial murder is a sex crime,” “a grotesque travesty of normal sexual functioning” (Schechter 9). Serial killers dream about the crime, as many would dream about sex, and then commit the crime after which they remain dormant for a period of time. During this time, their urges subside before building up again; this is the cooling off period. Such serial killers—“lustkillers,” says Schechter—are often psychopaths, individuals who are “morally insane” and have no regard for other humans as anything other than tools for personal gain.

The general consensus on the typical serial killer is as follows: … a white male between the ages of twenty-five and thirty-five.

He is not psychotic but rather psychopathic, suffering from what is often referred to nowadays as “Antisocial Personality Disorder.” He is most probably an extreme loner—a socially maladjusted misfit with few, if any, meaningful relationships. Cut off from the world of normal human connections, he indulges in particularly vivid, highly perverse fantasies of torture, domination, and murder. At some point, he crosses a line and acts out these fantasies on actual victims.

(Schechter 22) … a white male in his late twenties or thirties who targets strangers encountered near his work or home. These killers tend to be sociopaths who satisfy persona needs by killing with physical force.

(Fox 407)

That is, most serial killers kill not out of anger, necessity, or survival, but out of the pleasure they take in the kill, just as a rapist rapes for the pleasure of the act. They have complete apathy for the consequences of their actions, as jail time or guilt mean nothing to them. They are, in the true sense of the word, psychopaths. This is the type of human that most closely matches the construct of “ the serial killer,” a mythologized, inhuman monster with no regard for life.

III. Media Portrayal There has long been an eerie fascination with serial killers, before they were even termed “serial killers.” Francisco Goya in the eighteenth century created a number of engravings that showed atrocities comparable to those perpetrated by modern serial killers (Schechter 123). Also, artists in the late nineteenth century produced “broadsides,” which were “one-page accounts of sensational news events, the vast bulk of which dealt with shockingly violent crimes” (Schechter 2-3). In a modern culture of twenty-four hours a day, seven days a week, news reels, “our tendency to mythicize serial killers—to see them not as predatory criminals, but as creatures of superhuman evil—is reinforced by the media’s habit of tagging them with lurid nicknames,” a custom as old as “Jack the Ripper” (Schechter 102). The serial killer “belongs to the realms of both reality and fiction,” and it has “become an icon of pop culture, or rather, of US popular culture,” which is not surprising considering the United States contains “74 percent of the world’s serial killers, while Europe claims only 19 percent” (Allué 7-8). There is no single reason behind why there is such an obsession—that is really the only term for society’s macabre attraction—with serial killers, and psychopaths as well.

We might find his shameless risk-taking vaguely enviable, an

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exaggeration of impulses which we share, yet remain baffled at his self-destructiveness, the way he repeatedly and carelessly pursues courses of action which run directly counter to his own interests […]

(Elliott, Carl 90)

Furthering the popular fascination is the recent rise of intimate studies on the serial killer and the recent attempts to deconstruct him into a mental disorder—psychopathy—and into the causes of that disorder, which may include head trauma, childhood environment, and hormones and genetics. There is a certain element of incredulity at the inexplicability of the serial killer, that despite ongoing efforts to understand him, he remains a mystery shrouded in cruelty, described best by Schechter as “superhuman evil.”

Allué argues that serial killer fiction and film in particular “offer their readers or viewers […] the pleasure of pattern-discovering” (Allué 7). However, the fault of the serial killer genre as a medium of entertainment because of its pattern-discovering opportunities is that the patterns it presents must be simple enough for the average reader to find and understand. Unlike real serial homicides, in which there oftentimes simply is no pattern, and no answer, serial killer film and fiction must pander to the reader’s desire to “play detective,” so to speak. By doing so, serial killer film and fiction flattens and reduces the serial killer to a few traits. While there would be little problem in the existence of a few pieces of reductionist literature on serial killers, there are entire genres devoted to the serial killer and the psychopath, collectively diminishing the importance of the complexity in explaining any human being.

Unfortunately, the level of understanding of the human psyche that is required to understand why serial killers do what they do is impossible for scientists at this time. Many psychiatrists and sociologists have attempted to “trace the origins of individual development,” not only in serial killers but in the general population, yet doing so would make these sciences susceptible to the same “fallacy of reducing all experiences to one condition of their origin and so killing meanings by explanations” (Anandalakshmy 1115). This is especially true in recent years, with the development of better methods of gene analysis, and in their eagerness to understand the humane psyche, social scientists may use genetics to oversimplify the human brain and ignore the complexities it contains.

Another problem the media presents is inseparable from the media itself. Essentially, there is something fallible in what modern media is. Contemporary forms of entertainment, ranging from the news to literature to film, are all to some extent sensationalistic nonsense that are designed to increase ratings and viewership. On a larger scale, this is reflective of society’s gradual desensitization (Black 780), caused by the increasing availability of horrific reports from halfway around the world. In the context of the serial killer, the media’s tendencies towards dramaticism only exaggerate the singularity they place on the origins of the serial killer, further diminishing the actual complexities at play.

IV. Antisocial Personality Disorder

The majority of serial killers are psychopaths, and the “average” serial killer has been described as “psychopathic” (rather than “psychotic”) and of sound mind (Schechter 22).

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Psychopathy, although it has been widely replaced by “antisocial personality disorder,” is a term that persists in both psychiatric and criminal fields. After all, there is a significant difference in connotation between “antisocial personality disorder” and “psychopathy.”

Whereas one suggests a treatable mental illness, the other connotes the common media image of a serial killer, one that is remorseless and moral evil.

[Psychopathy may be a term] less similar to diagnostic terms […] than it is to moral terms […] Given the definition of psychopathy,[…] “psychopathic” would fit comfortably along evaluative terms such as “remorseless” or “coldhearted.” And psychopathy by almost any definition differs substantially from many other medical conditions, even psychiatric ones: its victims are not distressed by it; its pathophysiology is unknown; it is diagnosed entirely by behavioural [sic] criteria; and attempts at treatment meet with dismal lack of success.

(Elliott, Carl 89)

Antisocial personality disorder is one of many personality disorders, which, “unlike schizophrenic and mood disorders, do not have well-established biological markers and do not evidence predictable responses to treatment” (Rogers 678). The lack of “biological markers” forces psychiatrists to evaluate patients for the disease based on behavior alone, which is more erroneous and subjective.

The “absence of guilt and other moral emotions is one of the most consistent and longstanding features of the psychopathic disorder and its historical predecessors” (Elliott, Carl 89). However, psychopathy and antisocial behavior are “a complicated phenotype” (Caspi 852), with differing definitions from differing institutions. The official diagnostic criteria for antisocial personality disorder include “a pervasive pattern of disregard for and violation of the rights of others occurring since age 15 years” and evidence of “Conduct Disorder,” the consistent breaking of rules or laws, ranging from “[staying] out at night despite parental prohibitions” to physical cruelty to animals or humans (American Psychiatric Association 706).

Furthermore, the subject must be eighteen years or older for the diagnosis to apply. This definition seems rather arbitrary—why thirteen years of age for the onset of Conduct Disorder (American Psychiatric Association 98), why fifteen years of age for “disregard for and violation of the rights of others” (American Psychiatric Association 706), and why must a patient be eighteen years or older to even receive the diagnosis? This definition does nothing to clarify what a psychopath is. If anything, the American Psychiatric Association only further mythologizes him by breaking him down into patterns of unexplainable behavior and arbitrary criteria.

Blair makes a differentiation between antisocial personality disorder and psychopathy, referencing the 1991 definition by Robert D. Hare in which he described psychopathy as “a developmental disorder characterized in part by callousness, a diminished capacity for remorse, impulsivity, and poor behavioural [sic] control” (Blair 566). The Hare Psychopathy Checklist has been a “reliable” method of diagnosing psychopathy using this very definition, pinpointing behaviors such as deceitfulness, lack of remorse and/or empathy, impulsivity, and shallow affect (“a genuine ability to feel emotions”) as the markers for psychopathy (Fischette 1430).

Statistically, Hare’s definition contrasts with that given by the American Psychiatric Association, which are “poorly specified” and result in an APD diagnosis for 80% of criminals incarcerated, while Hare-defined psychopathy exists in only 30% of prisoners and less than 1% of mainstream education (Blair 566). Hare’s definition is also different in that it removes the

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arbitrariness with which the APA describes sufferers of antisocial personality disorder, and it accounts for the emotional and mental sources behind “Conduct Disorder” and other patterns of rule violation, citing the source of the behavior—impulsivity, diminish capacity for remorse— as symptoms for the disorder rather than solely the behavior itself.

But simply identifying symptoms of a disorder does not treat it, and psychiatrists and researchers must look towards the origins of the symptom to effectively combat it. While there is no evidence of biological markers, there are a multitude of theories on the causes of antisocial personality disorder, among which include “abnormalities in the development of nervous system,” in which serotonin is implicated, and negative “social and home environments” (Black). Because the sources of antisocial personality disorder are disputed, there are “farranging judgments […] about ‘psychopaths’ on matters such as dangerousness, recidivism, and treatability,” and the “validity” of the criteria set forth by the American Psychiatric Association is “seriously questioned” (Rogers 678). However, by examining these factors in both the physical sciences and the social sciences, researchers and psychiatrists can begin deconstructing psychopathy into its components to find ways to possibly prevent and treat it, and with the deconstruction of the psychopath comes methods to improve the criminal justice system and its attitude towards psychopathy.

V. Origins of Violence a. Head Trauma As early as 1937, when Cornell professor Dr. James Papez suggested the innovative idea that “emotions have an anatomical substrate, namely, the limbic lobe of the brain,” there has been increasingly credible evidence to support that human behavior can be deconstructed into the corresponding parts of the brain (Elliott 85). In the past eighty years, the validity of the correlation between the brain and human emotions has grown, as has the validity of the idea that harming the brain may result in changes in behavior. With these stipulations come the deterioration of the institution of free will, especially when head trauma can be directly linked with violent behavior that may cause some to kill. Can these individuals be blamed for murder?

There has been clear evidence of the connection between brain trauma and changes in behavior, particularly negative changes in behavior. That is, “aggressive behavior is not uncommon after serious head injuries” (Elliott 85), and criminal behavior “often springs from some combination of disinhibition, impaired social judgment, hyper-sexuality, aggression, and/or violence,” all of which can be caused by brain injury (Martell 320). An example of altered behavior that tends towards violence is episodic dyscontrol syndrome, which is often “a sequel of severe head injury” (Elliott 88). Symptoms include “recurrent attacks of uncontrollable rage, with or without external provocation (Elliott 88).

There are two types of emotional responses, spontaneous and controlled (Blair 562).

Spontaneous emotional expressions are unaffected by societal norms while controlled expressions result from both a biological response to emotional stimulus and a formulation of what is socially acceptable as the “proper” emotion. Researchers believe that while both spontaneous and controlled expressions seem to be related to the frontal cortex and the basal ganglia, an injury to the basal ganglia would result in decreased spontaneous expression and an injury to the frontal cortex would result in a decreased ability to “suppress an emotional

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expression” (Blair 562-563). This may result in exaggerated spontaneous emotions, like rage, and damage to the prefrontal cortex—the most anterior area of the frontal cortex—can cause violent, antisocial behavior. In the famous case of Phineas Gage, “the equilibrium or balance, so to speak, between his intellectual faculties and his animal propensities, seems to have been destroyed,” after being impaled by an “iron tamping rod” through the “frontal cranium” (Moffitt 110).

[He became] fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operation, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. A child in his intellectual capacity and manifestations, he has the animal passions of a strong man…In this regard, his mind was radically changed, so decidedly that his friends and acquaintances said that he was “no longer Gage.”

(Moffitt 110-111)

The damage to his prefrontal cortex “transformed him, virtually overnight, from a taciturn, reliable foreman in a railroad construction crew to a coarse, disinhibited unstable individual who was never able to work again” (Sapolsky 1793). His post-injury behavior is consistent with the symptoms of antisocial personality disorder (APD), suggesting that head trauma can trigger behavior that mimics antisocial personality disorder, or that head trauma can even breed APD. b. Hormones and Genetics Since the 1970s, scientists have begun establishing that there is some link between hormones, genes, and aggression. The persistence of aggression through generations and generations can be traced to the evolutionary advantages in “reproduction, protection of the young, and food acquirement” (Guo 545). However, the same aggression that allowed huntergatherers to survive is also the root of violence in contemporary society. Defined as “intentional injury to person or damage to property” (Davies 27), or as “an act intended primarily to cause injury or death of the target” (Bernhardt 45), aggression is often a precursor to a life of crime and, in some cases, murder.

Androgens are a class of secondary hormones in the human body that cause the emergence of male secondary sex characteristics. Because there is a positive correlation between testosterone, the primary androgen in the human body, and aggression, testosterone has been accepted as one of many hormones that cause aggressive behavior. Males have about four times as much testosterone as females, and the positive relationship between testosterone and aggression not only explains why males are more aggressive but may also explain why the large majority of serial killers are males. Aggressive behavior that results from elevated testosterone levels may also explain why serial killers are often between the ages of 25 and 35, an age range during which testosterone peaks. The potency of testosterone as a stimulator of aggression was proven in an experiment where laboratory mice were injected with testosterone. At maturity, two mice were placed in the same cage. In almost all instances where two male mice were in the same cage, there were substantial fights for dominance. Meanwhile, female mice fought in only twenty-eight percent of the cases (Davies 33). The drastic difference between the frequency of fighting and injuries is evidence of the direct relationship between testosterone and aggression.

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Catecholamines are steroids in the body that act as hormones or neurotransmitters and include serotonin, dopamine, epinephrine, and norepinephrine, all of which are related to pleasure. Serial killers and other career criminals are very similar to drug addicts in the level of catecholamines in their brain as they commit their acts. Drugs like nicotine and methamphetamine trigger the “reward system” in the brain by suppressing the inhibitors of dopamine, making the intake of such drugs pleasurable. In non-addicts, food creates the same sort of pleasure (Wise 1154). Similarly, criminals—especially serial killers who kill for some sort of release—that take pleasure out of violence and crime often become career criminals to experience the same “high” over and over again. However, as they commit more and more crimes, they become desensitized to the feeling of pleasure and need a greater stimulation to achieve the same high, and so they begin to commit more and more gruesome crimes in hopes of gaining that high. The desensitization to these neurotransmitters responsible for pleasure may partially explain why many serial killers have a compulsion to kill, and to kill more than once.

Just as addicts have a need for their drugs of choice, serial killers have a need for murder.

Scientists are also researching monoamine oxidase levels in the body to determine the origin of serotonin-based aggression. There are two types of monoamine oxidase (MAO), A and B, both of which catabolize catecholamines, yet only one has been definitively linked to aggressive behavior: MAOA. MAOA is known to lower the level of serotonin, a catecholamine known to cause aggressive behavior, in the body, thus reducing impulsive and aggressive behavior. In one experiment where laboratory mice were injected with an MAOA inhibitor, MAOA-deficient mouse pups show “a dramatically altered serotonin metabolism and severe behavioral alterations, both phenomena being linked” (Cases 1766). These “behavioral alterations” included aggression, which was measured by number of skin wounds in mouse pups housed in the same cage. While unaltered, wild-type mice were unwounded, a large percentage of MAOA-deficient mice showed skin wounds.

(Caspi 1764)

“All Tg8 pups [or pups with a deficiency in MAOA] displayed the same pattern of altered behavior, which varied with age. Chronic administration of the serotonin synthesis inhibitor […] reversed to normal all behavior traits of Tg8 pups” (Cases 1764). That is, when a compound that decreases serotonin is removed from the body, serotonin level increases, as does

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aggression, suggesting that serotonin is linked closely with aggression. This is further proven in the subsiding of aggression after natural serotonin levels are restored. In another experiment, “aggression was normalized by restoring MAOA expression” (Caspi 851).

While laboratory mice are imperative to research, particularly in this field where experimentation with human subjects would be unethical, there is one factor that must be studied for which mice cannot account: gene and environment interplay. But by comparing behavior of individuals who already have a defective MAOA gene—MAOA-L (“low-type”) individuals whose MAOA enzymes are not as effective or fail at catabolizing serotonin—with their individual histories, scientists are able to infer the correlation between genetics and environment. The general consensus is that a MAOA-deficiency is more relevant in cases where there is also a history of abuse or maltreatment (Caspi 852, Cicchetti 17325, Legrand 146).

Caspi in particular investigated “gene-environment interactions” by studying individuals with varying histories of childhood maltreatment between the ages of three and eleven years and with varying MAOA activity. The results are charted below.

Caspi 582 In the MAOA-L group, there is a much greater gap between individuals with no or probable maltreatment and severe maltreatment, suggesting the low MAOA activity contributed to exacerbating the symptoms of abuse, which included conduct disorder, violent and/or criminal behavior, or symptoms of antisocial personality disorder. That is, while childhood maltreatment slightly elevated the chances that an individual will be violent or antisocial, childhood maltreatment and low MAOA levels together greatly elevated the chances for violence and antisocial behavior.

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Both genes that code for the MAO enzymes are closely linked on the X chromosome, which may be another reason behind why there is a drastic difference between the number of male serial killers and female serial killers. Females have two X chromosomes. If a defective gene lies on the X chromosome, females have only a fifty percent chance of showing the phenotypic characteristics of that defective gene. However, because males only have a single X chromosome, they have a one hundred percent chance of displaying the characteristic.

Therefore, genes like the MAO genes are more frequently expressed by males than by females, and this may be one of the reasons behind why there are so many more male serial killers than female.

The problem with citing androgens, catecholamines, or genetics as the sole source of the serial killer is that biologists have not definitively connected—and likely will never connect— such biological factors to violent behavior. Although biology can influence biological tendencies, there is no guarantee that someday, it will be possible to examine an individual’s genes or hormone levels and declare with certainty that he or she will become a killer, or even a career criminal. The degree of expression in the mutation of the MAOA gene varies from individual to individual. Although those with a particularly low-active MAOA gene have a much greater chance of violence, as they are more impulsive and have fewer inhibitions to their desire to maim or kill, many individuals with a monoamine oxidase A deficiency express aggression to a lesser extent and come off as “competitive” or “domineering,” rather than “aggressive” and murderous: Aggression may be seen as an element of competitive behavior, particularly competition for sexual partners or the control of environmental resources… Extending the concept still further, aggression can include various kind of “take charge” behavior, such as energetic initiatives of a leader…

(Hodgson 482)

While high testosterone or a low-active MAOA gene likely do not cause aggression or murder, it may result in increased engagement in risky behavior that may lead to brain damage that could affect the frontal cortex, which could exacerbate any existing, underlying tendencies to aggression and risk-taking. In such a case, the damage to the brain would be more important as a cause of aggressive behavior rather than the low-active MAOA gene. There are so many uncertainties, proven by the simple fact that not all such individuals with high testosterone levels or low-active MAOA genes become serial killers, or even career criminals, even though many criminals exhibit such traits. c. Childhood Environment An element that is indispensible to examining the serial killer—and even to examining the average man—is his childhood. Among the “Ten Traits of Serial Killers” that Schechter gives in The Serial Killer Files, there are three that pertain to childhood environment: 4. They come from deeply troubled families. Typically, they have been abandoned at an early age by their fathers and grow up in broken homes dominated by their mothers.

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6. As children, they suffer significant abuse—sometimes psychological, sometimes physical, often sexual. Such brutal mistreatment instills them with profound feelings of humiliation and helplessness.

7. Because of their resentment toward their distant, absent, or abusive fathers, they have a great deal of trouble with male authority figures.

Because they were dominated by their mothers, they have a powerful hostility toward women.

(Schechter 22)

That is, the typical serial killer would have had an unhealthy relationship with one or both of the parents. Even though “these traits were extrapolated from a small sample of thirty-six sadistic lust-murderers, all men and most of them white” (Schechter 23), there is a consistent correlation between childhood maltreatment and aggression. Schechter explains this connection between childhood maltreatment and aggressive behavior in adulthood as follows: It makes perfect sense […] that if human beings are raised in warm, loving households—if they are brought up to believe that the world is a secure and decent place—then they will grow up with a health relationship to themselves and other people, able to give love freely and receive it in return.

Conversely, if a person is severely maltreated from his earliest years—subjected to constant psychological and physical abuse —he or she will grow up with a malignant view of life. To such a person, the world is a hateful place, where all human relationships are based, not on love and respect, but on power, suffering, and humiliation.

(Schechter 251)

However, simply “making sense” does not constitute evidence of a correlation between childhood abuse and violence. It is the numerous studies in which childhood abuse is directly linked with an elevated risk of violent and antisocial behavior that is evidence.

Childhood maltreatment is a universal risk factor for antisocial behavior. Boys who experience abuse—and, more generally, those exposed to erratic, coercive, and punitive parenting—are at risk of developing conduct disorder, antisocial personality symptoms, and of becoming violent offenders. The earlier children experience maltreatment, the more likely they are to develop these problems.

(Caspi 851)

Hare, of the Hare Psychopathy Checklist, admits that “violent psychopaths are more likely to come from violent households than are psychopaths whose behaviors are non-violent” (Fischette 1434), suggesting that even if childhood environment does not directly cause psychopathy, it at least influences its expression.

To a lesser extent, family cohesion is an important factor at play in aggressive and antisocial behavior. After all, abusive households often share a sense of destabilization of the family structure and a collapse in traditional family bonds. For example, there are drastic differences in the prevalence of psychopathy between English- speaking countries and East Asian countries, where English-speaking countries have a similar prevalence of 3.2% and East

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Asian countries have a drastically lower prevalence of 0.14% (Fischette 1435). The substantial difference between the percentages of psychopaths in the different cultures is likely the result of the difference in familial structures. Cultures in which the father figure has a particularly predominant role in the family hierarchy and where “family cohesion” is integral seem to “discourage psychopathy” (Fischette 1435). In such cases, it is not the society but the society’s attitude towards the family that discourages psychopathy, where cultures in which family bonds are more valued decrease the chances of psychopathy.

VI. Legal Implications There are varying opinions on whether criminal behavior can be predicted. Until not too long ago, the homicidal triad—bedwetting, fire-setting, and animal cruelty—in adolescence had long been used as an indicator of a life of crime as an adult (Diamond 442). While children who demonstrate a large concentration of the aforementioned characteristics—head trauma, childhood maltreatment, “mean genes”—are statistically more likely to commit violent crimes, there is simply no guarantee that they will or will not become psychopaths, career criminals, or serial killers. Bernard L. Diamond touches upon the greatest problem with predicting violent behavior with: “the prevalence of similar signs and symptoms in people who never commit a violent act” (Diamond 441). Diamond also argues that there is no way to tell if psychiatrists can “predict danger with reasonable accuracy” and that there are no “well-established clinical symptoms which, if present, can be relied upon to indicate potential danger” (Diamond 440).

Not only is it impossible to predict violent behavior with no margin of error, it is also impossible to rehabilitate psychopaths after their crimes. “Psychopaths […] are significantly more prone to violent crime and recidivism than non-psychopathic offenders, and the disorder is widely understood to be highly resistant, if not immune, to treatment” (Ells 158). That is, psychiatric professionals simply cannot offer the “100% guarantee” that psychopaths—or, in fact, any sort of violent offender—will not commit their crimes again (Coid 1582). “Inpatient treatment of psychopaths is notoriously difficult and can be physically and emotionally hazardous to the staff concerned” (Coid 1581). In one case in Scotland, two psychopaths who had been in an institution for their disorder had escaped and then committed a series of murders, despite receiving in-patient treatment, significantly lowering staff morale.

The criminal justice system is no more effective at rehabilitating the psychopath, and “no punishment is likely to make the psychopath change his ways” (Elliott, Carl 89).

Furthermore, it is unlikely that psychopaths will ever be considered legally insane: Psychopaths do meet current legal and psychiatric standards for sanity. They understand the rules of society and the conventional meanings of right and wrong. They are capable of controlling their behavior, and they are aware of the potential consequences of their acts.

(Fischette 1435)

Fischette is correct on all but one statement: “They are capable of controlling their behavior.”

Are they? Serial killers feel a need to kill, just as addicts feel a need to take their drugs of

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choice. The fact that serial killers simply enjoy their gruesome crimes only decreases the likelihood that they will ever be institutionalized instead of incarcerated.

However, the impossibility of predicting or correcting psychopathic behavior has not stopped the public from wanting a sense of security from the most prolific killers of modern society. Because there is an inherent fear of change in human society, there will always be an urge to discover and understand the psychopathic serial killer, to understand why he does what he does, and to find ways to stop him.

VII. Conclusion In the CBS crime drama series Criminal Minds, season 3, episode 14, “Damaged,” there is an interview between two of the FBI’s criminal behavior analysts and a serial killer, culminating in an instance when the serial killer, Chester Hardwick, was prepared—and able— to kill the two agents in order to escape death row. The guards were making their rounds, and there would be no one to answer the door to the interview room, which was locked from the outside. To escape certain death at the hands of a sadistic lust-killer, one of the agents, Spencer Reid, began to ramble on the one thing that had plagued Hardwick his entire life—the reason that caused him to brutally murder women over and over again. Reid references that Hardwick’s parents were both mentally ill, his mother bipolar and his father clinically depressed with posttraumatic stress disorder. Hardwick’s parents “beat each other as much as they beat [him], so violence became a natural expression of love.” Reid also references the “hypothalamic region of the limbic system,” the “most primitive part of the brain” that “wants what it wants without conscience and without judgment.” In most children, it is countered by “a normal relationship with their mothers,” but Hardwick’s had never learned control. Finally, Reid ends by stating that although Hardwick had said his victims never had a chance, it was Hardwick who never had a chance. However, as the agents leave, imminent danger subsided, Hardwick questions, “Is that true, I never had a chance?”

Reid replies, “I don’t know, maybe.”

Although Criminal Minds is a fictional television series that, like other forms of modern media, is designed to sensationalize and dramatize, these two lines of dialogue—“Is that true, I never had a chance?” “I don’t know, maybe.”—capture the essence of the debate on serial killers and psychopathy. There is no definite reason, no identifiable source, for why serial killers do what they do, and there is no evidence that individuals with a certain combination of traits are “doomed” to become violent offenders. On the other hand, there is also no evidence that some individuals without any factors for violence will not become violent or will not become killers. While the media tries to reduce the serial killer into one or two parts, the truth of the matter is that the human psyche is too complex. All parts and factors are important, and any reduction taken will diminish the quality of the profile.

That is not to say that all factors for the creation of the serial killer are equal. All “true” serial killers, who differ from mass murderers in their sadistic desire to kill, are psychopaths, suggesting psychopathy—or antisocial personality disorder—is essential in the makings of a serial killer. The confluence of a number of origins of psychopathy—head trauma, genetics, and childhood maltreatment—can further elevate the probability of violent and aggressive behavior.

Despite the connections to serial killing, there is still no method of determining whether the

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complete convergence of these three characteristics will positively result in psychopathy, and there is no definite guarantee that psychopathy will also lead to serial murder.

The improvability of the possible factors in the creation of the serial killer leads to implications in the criminal justice system. If there were a direct and obvious correlation between something like head trauma and serial killing, or that serial killers had no choice but to kill because of a gene that gave them a compulsion to kill, or that abusive relationships with their parents skewed any moral compass they had, then the decision to institutionalize serial killers would be easier to make. However, serial killers and other psychopaths like them are not legally insane; they understand the difference between the social constructed ideas of “right” and “wrong.” As such, and because it would be irresponsible to pinpoint a single source behind their creation, serial killers must be considered through all realms of science, biological or sociological, and law. Only by acknowledging each field’s influence on the construct of the serial killer is it possible to set forth on the road to understanding him.

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Bernhardt, Paul C. “Influences of Serotonin and Testosterone in Aggression and Dominance: Convergence with Social Psychology.” Current Directions in Psychological Science 6.2 (1997): 44-48. Print.

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Science, 297.5582 (2002): 851-854. Print.

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Hunt for the Heretic

Hunt for the Heretic: The European Witch Hunts as Religious Scapegoating Kiana Nedele, â&#x20AC;&#x2DC;12

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Hunt for the Heretic Abstract

Between the years 1560 and 1700, an unprecedented number of witch hunts and witch trials occurred across Europe. Although witch-hunts had occurred in Europe since the twelfth century, these first hunts were few and far between. But over four centuries later, the craze over witches reached an incredible height, as neighbor turned on neighbor and even the highest lords subscribed to beliefs of a Satanic conspiracy headed by witches. To understand this new phenomenon, several questions must be addressed. First, why did the hunts increase during this particular period rather than any other (most pressingly, during the 1300s, during the first ravages of the Black Death and the Great Schism)? And second, why witches?

To truly understand the widespread witch hunts of the sixteenth and seventeenth centuries, one must place them in the context of the cultural, social, and political events of the times. To blame such a massive phenomenon as this on any one reason (like misogyny or the lack of a scientific worldview) is to overly simplify the event without truly understanding its causes and motivations. The witch hunts were the result of the immense upheaval in nearly every facet of life—society, religion, and politics—over which the majority of people had little to no control. Powerless to provide any lasting stability to their lives, ordinary Europeans lashed out in the only way they could, manifesting the cause of their fears in something which they could physically attack. As religious strife deepened, beliefs hardened and became more extreme, heightening apocalyptic worldviews and making the dark side of religion, the witches and devils, seem all the more real. The religious tension and extremism caused by the Reformation and Catholic response provided the scapegoat of witchcraft that the average European so desperately needed on which to take out his frustration at the instability in all aspects of life.

Contrary to popular belief, witch hunts did not even exist for the majority of the Middle Ages, being “virtually unknown until the final centuries”1 of the period. The myth of the witch as known today did not solidify until the Renaissance, and witches were not systematically attacked until the period studied. These hunts occurred concurrently with widespread upheaval not just in technology or in politics, but in societal order and religion as well. The Reformation tore apart the unity of the Roman Catholic Church and destroyed all dreams of one united Christian Europe; in the years following it, as various sects spread and clashed with others, religious tensions grew and spread into outright war. Politics, too, became subverted by individual needs as Europe moved towards individual nation-states rather than the dream of a unified Christendom. As individual countries and dynasties strove for their own gains and no one else’s, the politics of the Holy Roman Empire, already split by religion, took a turn for the worse. The Thirty Years War, precipitated by religious strife and political tensions, soon became driven completely by the new self-serving politics of neighboring countries, tearing apart the Empire and destroying political and physical security. Concurrently, the Scientific Revolution took the humanist gains of the Renaissance even further, undermining the old world order and destroying what mental certainties still remained. This intellectual, religious, and political turmoil affected every aspect of peasants’ lives and removing the certainty of the old monolithic authorities.

With the Reformation, the medieval certainty of the Church and its God, which had united Europe with its surety for much of the past millennium, was suddenly wiped away within a span of fifty years. As if that were not enough, war broke out all over, ravaging the countryside where the very necessities of life were produced and decimating the population, thus removing what little surety of life the everyday peasant had. Previously if the promise of life were taken

1 Klaits 19

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away, one could turn to the Church, safe in the promise that at least the next life would turn out better than the last. But this promise was no longer there; not only did the Reformation destroy the certainty of the Church, but the Scientific Revolution worked to remove all former certainties of God as well in favor of constant questioning, a much more unstable spiritual lifestyle. In reaction to the loss of security, people naturally turned to tradition, either the tradition of the Church and its attacks on black magic, or to the Protestant tradition of purifying God’s message, which meant stamping out dissidents and practitioners of old magics. The view of village ‘witches’ moved to the extreme, portraying them as Satan-worshipping dark magicians rather than being harmless old women whose only powers went towards a placebo effect.

The witches were perfect targets to be made scapegoats, as they lacked any kind of systematic or even social protection. As both Catholics and Protestants took on more extremist beliefs, both camps sought to stamp out heresy and unorthodoxy at all levels, meaning there was no longer room for pagan/pre-Christian beliefs in the European lifestyle. The witches, last visible remnant of such practices, became the perfect target on which to blame society’s woes in the name of God. As a result, the witch-hunts, backed on all levels of society, raged unchecked while people sought a scapegoat for the misery and upheaval occurring. Only when Europe settled and the promise of stability returned with the end of war, the rise of secularism, and the Enlightenment, did the witch-hunts finally come to an end.

The first section of this paper will discuss the historical events during and directly preceding the witch-hunts and thus basing them in the events of the sixteenth and seventeenth centuries. The second section presents and then elides the thesis that the hunts were prompted by a need for scapegoating and that witches became the particular target as a result of religious extremism and the move for stricter orthodoxy within each belief system.

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Hunt for the Heretic Historical Background

The period between 1500 and 1700 was one of great change and widespread instability directly following a period of stabilization and growth. By 1480, Europe had at last largely recovered from the ravages of the Black Death (which current scholarship estimates to have killed about a third of the population2) and from the religious confusion of the Great Schism, which, at its height, had led to the existence of three separate popes all cursing and excommunicating each other. Through the Italian Renaissance, art and culture were ushered into a new celebration and appreciation of human talent and beauty, and the popes worked to regain their former might and power over culture and politics. Although the Renaissance did herald new human-centered approaches to art, politics, and even science, for the most part Renaissance thinkers continued to be good Catholics and not oppose mainstream thinking; the rise of humanist thought came with a new appreciation of the ‘God-given’ talents of reason and logic, which were seen as evidence of God’s preference for and support of human supremacy. The political map also remained relatively stable; the Hundred Years War had ended, and although various countries still strove for power, diplomats and kings alike tended to use legal methods rather than war to increase their influence. Overall, things were looking up for Europe. However, this illusion of certainty would soon be shattered by events of the next two centuries.

Under the veneer of recovered Papal power lay immense corruption and widespread spiritual malaise within the Church. Lay priests often lacked a firm understanding either of the Latin masses they recited or even of the religious doctrine that they were supposed to be teaching and protecting. Indulgences, originally meant to only reduce one’s time spent in purgatory for sins already forgiven, were sold as tickets to release a soul from Hell and send it straight to Heaven; this was a result both of the apparent greed and money-grabbing of the clergy but also was due to the lack of doctrinal understanding at all levels of the Church. Bishops abandoned their assigned parishes to court power elsewhere, and clergy at all levels flouted the vows of celibacy and temperance. The popes themselves practiced rampant nepotism, placing their ‘nephews’ (but more often their illegitimate children) in positions of power and electing children as young as ten to become cardinals. As popes focused on the power and art of this world, they increasingly ignored the religious dimension of their work. Although corruption had arguably reached its greatest heights a century earlier during the Great Schism, the Renaissance Church seemed set to rival such depravity; De Lamar Jensen notes that “by Leo [X]’s time, the curia itself was as corrupt as it had been in the days of Wyclif and Hus.”3 What had changed over the past century and a half were technology and the availability of information. The invention of the printing press meant the dissemination of knowledge on a level never before achieved since perhaps the glories of Rome in its heyday. The press “stimulated the creative processes of traditional scholarship as well as opening up possibilities for writing new materials totally unrelated to the problems of conventional and classical scholarship.”4 It also led to the rise of the first form of modern media—the newspaper’s parent, the pamphlet. Humanist thought led scholars to investigate problems or apparent paradoxes, like Lorenzo Valla’s expose of The Donation of Constantine as a fraudulent document forged by the Church. Church excesses and corruption thus became well known: Jensen notes that “little was

2

Jensen 3 Jensen 215 4 Cole 93 3

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hidden from the public eye”5, undermining Church stability and credibility. The Church’s inability to ever properly address such concerns lowered its standing even further.

Its stability and hold over intellectual thought was faltering as well. The new methodology formed by the Renaissance, which “combined three procedures, one logical, one experimental, and one mathematical,”6 would enable the next generation of scholars to not only formulate explanations to cover Aristotle’s weak points but to discard Aristotle altogether. In 1500, Church-approved scholarship still held, but humanist thought was providing the tools and expanded worldview that would soon lead to the findings of such men as Kepler, Newton, and Descartes, whose theories revolutionized the way people saw the world.

As a result, the continent was slowly spiraling downward in what G.R. Elton argues “can only be called a spiritual crisis.”7 The Church was not only corrupt and more focused on expanding its military power rather than saving souls; it simply failed to truly address the spiritual needs of the age. Because of this, Europeans of all social classes began to seek consolation elsewhere. Apocalyptic expectations increased dramatically, giving rise to “a devotional urgency that had not been seen in the church for over 200 years. ... People increased their ardor for meaningful religious expression,”8 but the Church utterly failed to deliver, both in terms of clerical devotion and in terms of perceived doctrinal promises. The Reformation sought to provide this meaning and this zeal.

In 1517, Martin Luther posted his 95 Theses on a church door in Wittenberg. This act alone did not cause the rift between Catholic and Protestant; Luther was merely protesting the act of selling indulgences, which (as has already been noted) had been perverted into the selling of one-way tickets straight to Heaven. The rift occurred when the Church overreacted against Luther’s protest and eventually tried to force him to recant. In doing so, they forced Luther to justify his reasoning thoroughly, and to do so he revealed his new theological treatises in all their glory. Luther argued that good works would not increase one’s standing in God’s eyes because, being God, He had no need for what paltry things individuals offered; thus one could never bribe one’s way into Heaven by doing good deeds. Rather, admission to Heaven depended solely on God’s will, which meant that the only way a human could hope to enter was through wholehearted faith in the Lord, a doctrine known as sola fide, or by faith alone.

Luther (and the Protestants to come) made full use of the new printing presses to spread the Word as they saw it. Thus, while the Catholics debated and the Emperor Charles V left Germany to combat the Ottoman Turks, Luther’s new ideology spread by means of the written word. It was demonstrative of the new form of Christianity: an emphasis on the actual writings in the Bible and on the importance of individual reading, which lead to an emphasis on universal literacy and translations into the vernacular tongues so that all could read and understand the holy text.

The Reformation quickly took off and left Luther’s control. Many absorbed his teachings, since Luther remained socially conservative and thus continued to support the princes and the overall existing political structure. Others, however, took his ideas to their logical conclusions.

The peasants revolted, citing Luther’s emphasis on individual equality before God to extend into this life, and many extremist splinter groups like the Anabaptists tried to form their own communes in which the word of God would be properly followed. Following Luther’s example,

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Jensen 217 Rice 18 7 Elton 28 8 Jensen 217 6

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the Reformers often “depended heavily on printed sources for communication and transmission of ideas”9; they took advantage of the new availability of the written word and produced pamphlets, tracts, and even the first satirical cartoons, all of which soon spread rapidly and inflamed all levels of society through the use of both word and image.

Other reformers, like Zwingli and Calvin, formed their own Protestant sects based on their own interpretations of the Bible. Zwingli agreed with Luther but went one step further, denouncing all Catholic pageantry and encouraging image breaking. Calvin focused on the idea of God’s will being the sole agent deciding whether or not one went to Heaven or Hell; he eventually formed the doctrine of predetermination, which holds that God has already chosen those who will enter Heaven, the ‘elect’, before they are actually born. This doctrine, although reaching the logical conclusion of Lutheran speculation, meant that one must trust completely in God and simply hope for the best. What Zwingli and Calvin significantly had in common, however, was that, unlike Luther, both were practicing preachers and both managed to institute their reforming doctrines in specific cities, thus creating a solid base of believers. These followers, just like the beliefs they followed, were each more extremist and zealous than the previous reformist group. Thus, as the Reformation spread and splintered, it also radicalized and hardened religious dissent and differences.

The Catholics were slow to form a Counter-Reformation, giving the Reformation time to spread and take root. However, when the Catholics finally got around to addressing corruption, the lack of education, and doctrinal disputes, they struck back with a vengeance, most notably through the Jesuits and the return of the Inquisition. Founded by Ignatius of Loyola (later canonized as a saint), the Jesuits were answerable to the Pope only and strove to spread the ‘true’ word of God no matter how difficult or dangerous. The Jesuits worked mostly through missions, which they established (by force if necessary) and at which they began educating the locals in the endorsed Catholic doctrine (as newly confirmed by the Council of Trent). These priests were trained not only in theology but also in more martial pursuits; even Catholics feared them for their semblance to an army of militantly righteous Fathers. Although their order had not been founded in direct response to the Reformation, the papacy soon put the Jesuits to good use in Europe as well as overseas. While the Jesuits corrected existing beliefs and tutored the next generation to grow up good Catholics, the Inquisition set to work stamping out heresy in any and all forms. The Inquisition especially attacked the new literature of the printing press, acknowledging the Reformers’ hold on it; all tracts which undermined Catholic unity of thought in any way (including new scientific finds) were suspect and often banned outright. Through better education of priests, better attention to Church abuses, and the new fanatical approach to religious unity, the Church made an effective counter-strike at the Protestants, winning back many territories and confirming that it was here to stay.

The zealousness of the Counter Reformation brought on early clashes with the new science being developed. Copernicus’s theories when first published in 1543 did not attract much attention partly because he had no evidence to back them up but also because the Church was still convulsing from the Reformation upheaval. But by the time Galileo published his own findings in the early 1600s, the Church’s response to the Reformation was in full force. In 1616, the Church, “owing largely to pressure from the Jesuits,”10 officially denounced Copernican heliocentricism. Galileo’s complete repudiation of Church-approved Aristotle and Ptolemy could only lead to trouble in such an environment; in 1632 he was put under house arrest after

9

Cole 98 Dunn 207

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publishing his Dialogue Concerning the Two World Systems, which mocked the Ptolemaic system and the Pope himself. The Church’s response was understandable: Galileo’s findings (like Kepler’s) challenged the very worldview to which Europe had subscribed for the last millennium. Until a fully comprehensive and explainable system came to replace the old Aristotlean system in the form of Newton’s 1687 Principia Mathematica, the intellectual world faced great uncertainty and instability—the old system was being torn apart, but without something to replace it, the world now seemed without order or reason. As a result, many turned back to religion as the answer to all problems.

As both sides of the religious split hardened their views and became more extremist, religion soon began to spill over into politics. Neither side was willing to compromise, especially not where it mattered most in doctrine, and both viewed the other as heretical and bound for Hell. There was no thought of coexisting; religion gave meaning to life, so to have someone deny that meaning was an attack not just on belief but on one’s very way of life. Various rulers tried to impress their own beliefs on their people with varying success. The results were the so-called religious wars that overtook much of the continent; political power plays had a major role in such wars as well, but religion helped exacerbate tensions even further. In England, Elizabeth I managed a successful Anglican compromise between Catholic and Puritan strains, though not without continued Puritan resistance, which later exploded during the English Civil War and the short-lived establishment of the Puritan Republic (really a dictatorship under Cromwell). The wars for independence in the Spanish-run Netherlands were also precipitated by religious and cultural conflict between ruler and local; the Spanish king was separated from his Dutch subjects not just geographically but culturally, linguistically, and religiously as well, and both sides were driven by religious extremism at various points in time.

The French wars of religion were even more brutal; the English managed to confine religious dispute, and the war was as much about kingly overextension and governmental dispute as it was about religion. In France, religion was the catalyst in a court already tense from the various noble families all jockeying for royal power. The French Calvinists, or Huguenots, and the ruling Catholic family fought for control of both state religion and throne. Huguenots were slaughtered left and right (most memorably in the St. Bartholomew’s Massacre), and the strife only ended when the new king Henry of Navarre (Henry IV) changed his religion back to Catholicism to win over the capital Paris and issued the Edict of Nantes, which protected Huguenots’ basic religious freedom.

In Germany, several Protestant princes joined forces to create the Schmalkaldic League.

What started as a religious alliance to oppose the emperor’s attempts to stamp out all religious deviancy soon turned into a territorial alliance that more generally fought against the expansion of Charles’s power at the expense of the territorial rulers under him. When first created, the League was very weak and uncoordinated; what saved it, and what allowed Protestantism to spread so far within the Empire, were the Hapsburg emperor’s many commitments elsewhere— in Hungary, the Ottomans under Suleiman the Magnificent pressed ever westward, and in Spain and its territories Hapsburg control was less than secure. When Charles V finally got around to stamping out all non-Catholics in the Empire itself, the Schmalkaldic League and its allies put up a fight. Eventually fighting was ended with the Peace of Augsburg in 1559, which ended the religious struggles in a tie, stating that the local prince in charge got to decide whether his territory would be Catholic or Lutheran. All other forms of Protestantism were excluded from the treaty.

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Here, as elsewhere, religion became yet another element in the conflict between territorial princes and the monarchs governing them, as each attempted to expand their own power at the expense of the other. None of the religious wars were entirely precipitated by religion only; preexisting power struggles still provided the main reasoning and motivation behind the conflicts. The introduction of religion most often merely hardened each side against the other and precluded any opportunity for compromise without bloodshed.

In Germany, the religious question seemed settled after 1559. However, the spread of variant forms of Protestantism meant that the official choice offered by Augsburg was no longer satisfying. But for the most part people worshipped as their rulers saw fit, and the minorities with different beliefs mostly coexisted peacefully without really disrupting the ordinary course of life.

This changed when Ferdinand of Styria, heir to the throne of the Holy Roman Empire, became king of Bohemia in 1617. A “rabid Catholic,”11 Ferdinand had no time for toleration. He quickly set about oppressing the local variant of Protestantism, the Utraquists. Although Ferdinand’s measures were legally correct, his heavy-handed approach and his underlings’ implementation were “deliberately provocative.”9 Peter H. Wilson notes that this dissatisfaction with means rather than the actual end meant that “politics polarized along confessional lines, since religion was the only ground on which to attack royal policy.”12 Once again, the political tensions of the region were exacerbated by religious tensions.

In 1618, the Bohemians declared revolt in the celebrated defenestration of Prague, throwing the king’s ministers out the castle window. Unfortunately for them, said king had just been elected Holy Roman Emperor and thus had all the resources and political might of that position. The rebels called in Frederick of the Palatinate to be their new king, a somewhat-fellow Protestant. However, Frederick brought no real allies with him, and his equally rabid Calvinist underlings soon were infringing on Bohemian culture just as much as Ferdinand’s ministers. The rebellion did not go well, and by 1620 Frederick’s armies had been chased out of Bohemia and back into his own lands, the Palatinate.

However, several others decided to capitalize on the war to gain more prestige or land for themselves at the Emperor’s expense, a pattern that would continue throughout the war.

Transylvania joined the fight in rebellion against the Emperor and was not subdued until 1626.

Meanwhile, a giant mercenary army on Frederick’s side (in word at least) fought the emperor’s self-serving ally Maximilian of Bavaria; as the emperor's armies pressed the Protestants north and Ferdinand's power waxed dramatically, the surrounding countries began to take notice. In 1625, King Christian IV of Denmark entered the war, purportedly as ‘defender of all Protestants’ but really in the hopes of personal gain at the expense of the Emperor. By the end of the war, France, Sweden, England, and Spain would all follow similar paths, either directly entering the war to lessen Ferdinand’s power and gain territory for themselves or by supporting the main participants with monies and men. Nearly everyone except the Emperor and the Empire’s actual inhabitants wanted the war to end later rather than sooner; it was a golden free-for-all opportunity for the Hapsburg’s rivals to drastically reduce their power both through money, influence, and territory. By 1648, Ferdinand’s opposition had succeeded in this goal. Although the territorial gains had been less than stellar, the Empire was in shambles, and the office of emperor little more than a name.

11 12

Dunn 83 Wilson 270

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Hunt for the Heretic The Witch Hunts

Between the years 1560 and 1700, between 30,000 and 60,000 people were executed for witchcraft.13 Unlike events of mass hysteria at other times in history, where the majority of those targeted were attacked all at once or within a short amount of time, the European witch hunts occurred over the span of a century and a half and were widely dispersed. Most hunts existed independently from each other, flaring up in different parts of Europe as individual villages all experienced the craze at different times. Many of the trials were limited to the local scale— villagers accusing each other or city dwellers accusing each other—but authorities with real rank often participated, either by beginning the hunts themselves or, more often, by coming in to investigate local worries. The witch-hunts thus encompassed all levels of society and were prompted by issues affecting all levels of society, not just one group in one place. To take the witch hunts at face value—individual attacks by locals on locals—is to overlook the shared commonality, the target and the impetus, and to overlook the witch craze’s ability to cross any and all class barriers.

This craze on all levels of society, ranging from the lowliest peasant to the local gentry and sometimes to the king himself, was due to the fetid mixture of religious upheaval and extremism, scientific experimentation and doubt, and the massive bloodshed and strife brought on by the many wars and political fragmentation of the period. The Renaissance had brought a semblance of order back to Europe, allowing it to recover from “the calamitous fourteenth century ... [and] the crisis of faith and despair associated with it.”14 However, the Reformation, Scientific Revolution, and Religious Wars completely destroyed the false security of the Renaissance, and the “course of the witch craze was directly affected by these momentous developments.”15 The loss of security in nearly every facet of life led to the subconscious yearning for a scapegoat, some group on whom to foist the blame and who could be punished easily enough. This scapegoat took form in the witches. Religious extremism and a yearning for security pushed Europeans to stamp out heresy and punish the wicked at every level, thus making witches and the unsanctioned magic they practiced a perfect target.

The security of the Renaissance was not in any way permanent. Although people continued to follow the leadership of the Church, a “grave lack of understanding of the religious and social problems of the time ... permeated the papacy,”16 widening the gap between layman and priest. Unfortunately, “fundamental changes in the relationship between faith and creed were ... taking place”17 as people’s religiosity and spirituality increased. They still wanted to believe in, and have the solid reassurance of, the Catholic faith, but the actual Catholic priesthood failed to satisfy, so many began unconsciously searching for alternatives; rites of devotion grew in popularity, as did the cults of the Virgin and of the Saints. The Church’s failure to service its people’s spiritual needs created a void which the Reformation set out to satisfy.

The impact of the Reformation was immediate and overwhelming; in a single stroke, Luther eradicated the unity of the Roman Catholic Church and undermined the one faith that had served Europe for the past millennium. The turmoil was unprecedented. But for those who subscribed to the new faith, the Protestants “clearly filled emotional needs that the established

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Waite 154 Jensen 3 15 Klaits 4 16 Jensen 197 17 Jensen 217 14

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church did not.”18 As a result, they clung to their new beliefs with all the fervor and zeal which had previously been channeled toward such activities as pilgrimages. Thus the Reformation was in many ways the violent culmination of the Renaissance shift toward personal devotion and selfchastisement.

The Protestants moved for a focus on the specific word of the Bible, a more individual interpretation of the Word, and the necessary translation of the Bible into the vernacular, together making the Bible more immediate and accessible to all people. This move towards individuals connecting directly with God and the accompanying attack on Catholic pageantry questioned the very existence of the Catholic Church. Priests were meant to serve as intermediaries between lay people and God, but if the ordinary folk could directly access the Bible, they could directly access the Lord as well, making the priesthood highly unnecessary. By extension, the Church, arguably the primary institution governing Europe for the past thousand years, was itself unnecessary as well. The resulting upheaval was understandable; in a few years, the very institution on which all lives depended had been tossed aside and decried by all manner of thinkers who based their arguments on common sense and popular ideals. It had been one thing for humanist attacks on Church excess and corruption, since similar movements had been occurring throughout the Church’s history. The Reformation, on the other hand, “was a revolution”19 and was thus “extraordinarily destructive.”20 The result was that “for the first time in many centuries, problems of religious choice and conversion became of major concern for ordinary men and women,”21 forcing a “personal drama of conscience”22 that left many even more doubting and confused.

In addition, the Reformation wreaked havoc on the societal order as well by necessitating the creation of new churches and religious institutions and, with more radical sects, involving the reorganization of city governance as well. Church lands were seized and redistributed, and Calvin’s Geneva was reordered into as close as he could get to his ideal religious community.

The Peasant War of 1524-6 brought to the fore another part of the Reformation’s social effects.

The peasants took Luther’s ideals about equality before God literally and revolted, arguing that social distinctions ought to be abolished and demanding redistribution of gentry land amongst the people who actually worked it. Luther himself quickly backtracked from such a radical stand, but these ideals soon manifested themselves in other splinter Protestant groups. Thus the Reformation undermined not only the spiritual certainty and unity of the Catholic Church but threatened the very structure of society as well.

Intellectual security was just as scarce. What had begun in the Renaissance as simply an attempt by the humanists to update the Aristotelian-Ptolemaic worldview soon turned into a total revamping of the perceived world order as the new thinkers “obliterated the traditional view of nature.”23 Kepler and Galileo threw out the old geocentric model of the universe and proved the Copernican system mathematically, and Galileo’s work in physics destroyed Aristotle once and for all; such findings clashed especially with the Catholic Church, further undermining spiritual certainty as well. Meanwhile, philosophers like Bacon and Descartes argued for an entirely new approach to how scientists even considered the world, championing respectively the inductive

18

Rice 149

19 Rice 152 20 Matheson 13 21

Rice 177 Rice 179 23 Dunn 200 22

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and deductive methods of reasoning. The result of these attacks on all aspects of the old world order was “an era of dissolving certainties”24 which began in the Renaissance and which the Scientific Revolution only exacerbated further.

What made the Scientific Revolution so destabilizing was its inability to replace the worldview it threw out with a new comprehensive system that entirely replaced the old one sanctioned by the Catholic Church and provided just as much security. Kepler and Galileo found new equations for specific cases but never produced an overarching order that comprehended seemingly all parts of the natural world. This system came in the form of Newton’s Principia Mathematica, which was not published until 1687. Thus for nearly the whole period, science existed without any stabilizing theory to explain the world as a whole. Although the average peasant might not have been very aware of such academic upheaval, the elites in charge certainly were, and the new advances in science “forced men to reframe their religious beliefs”25 in order to reconcile their old God with the findings of the Scientific Revolution. Many chose to cling all the more desperately to their religions and overthrow science altogether, an undertaking which itself brought insecurity by bringing people back to the unsettling question of religion and religious choice.

Politically, “the forces of feudal decentralization and monarchical centralization were in precarious balance,”26 and during the sixteenth and seventeenth centuries the balance slowly shifted towards the monarchies. The price was nearly a full century of warfare, as territorial lords belonging to various factions of the more decentralized Protestantism struggled with their Catholic kings for control. The old feudal order, weakened by the Black Death and even more by the Renaissance tendency towards consolidating power, finally met its true end during the wars of the sixteenth and seventeenth centuries, as the main power of the lords were broken and centralized government gained ascendancy.

What made these wars all the more brutal was the added religious component. In addition to genuine conversions, religion often served a specific political purpose as well. Protestantism emphasis on the individual offered territorial lords justification and approval of their own struggles for individual power and prestige, and the regionalism of the new Christianity provided them with a religion whose organization they could personally control. Catholicism, on the other hand, was the choice of many kings, especially those whose families had long held power. The Roman Catholic Church quickly came to represent conservatism and stability rather than the philosophy of skepticism fostered in Protestant lands. Religion thus became both motive and tool in the struggles between king and peer.

When the Reformation began, there existed no such thing as religious toleration. (The only reason the Peace of Augsburg later held as long as it did in Germany was that, for the most part, religion only really varied from one prince to another; where a religious difference existed between peasant and ruler, conflict soon followed, most notably in the Bohemian Revolution that triggered the Thirty Years War.) Both sides’ beliefs were a complete contradiction of the other’s worldview, and since one’s one view must be right and thus all opposition headed for hell, each side felt entirely justified in ridding the world of heretics and deniers of God. Mattingly points out tellingly that “in wars of ideas, the sense of proportion, like the knack of compromise, is easily lost.”27 Many in power on both sides of the religious split felt that it was their Christian

24 Elton 29 25 26

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Mattingly 167

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duty to impose their truth on all others around them, but dissidents felt the same about their own beliefs, so that, in particular with a Calvinist minority, “any attempt to enforce conformity to Rome meant civil war.”28 As a result, “a very ugly situation hovered uneasily between social revolution and mass slaughter in the name of Christ.”29 Unfortunately for Europe, the situation quickly moved to mass slaughter, and it would take much bloody fighting to finally achieve peaceful coexistence.

Eventually, kings rather than regional lords won power, but not after a prolonged struggle, and not until religious toleration and coexistence became the norm (if only because people finally grew weary of killing). This power shift and the accompanying wars prevented ordinary life from ever really stabilizing. War involved not only pitched battles but the drafting of local men to fight, rampant looting and pillaging (and sometimes worse) of all regions the armies passed through, and the spread of diseases carried by the army. The most notable of such conflicts was the Thirty Years War. Here, the move towards monarchical centralization was successfully countered by the international intervention and extended combat; on the regional level, princes continued to consolidate their power at the expense of the gentry and lesser nobility under them. However, just as in the other religious wars of the age, while the war was actually going on, society faltered and there occurred a “partial breakdown of government in many areas.”30 War not only destabilized society; in the areas directly affected, war often temporarily destroyed society.

The Thirty Years War, though particularly brutal, was indicative of the general pattern of war during the period. Marked by “brutality, plunder, murder of civilians, plague, ... war taxation and population displacement,”31 war involved the deployment of massive armies (mostly mercenaries from other countries) that stayed constantly on the move, getting sustenance (food, clothing, money) from the lands passed through by means of brute force. Sustained by conquered territories, armies thus forced the costs of war onto the enemy economy.32 The shifted economic burden, accompanying destruction, and civilian population loss all led to economic stagnation and in some cases outright downturns as well as meltdowns.

Peter Wilson notes that as result of continued combat in the Thirty Years War, “the extensive operations and rapid reversals of fortune fostered a climate of uncertainty,”33 and the same held true for the wars of religion elsewhere on the continent. The Thirty Years War was particularly devastating since it lasted for so long and, after 1632, the war “rapidly spread ... into all parts of Germany.”34 The war was seen as the epitome of senseless destruction, becoming a “benchmark for atrocity elsewhere in Europe”35 even before the war had ended. An estimated 8 million died from war or complications arising from it (disease and starvation), over 20% of the Empire’s population.36 However, similar happenings occurred through the continent wherever politics and religion precipitated war. Because war overturned every aspect of life (health, economics, food supply, and political order), it was incredibly destabilizing. To the ordinary

28 Mattingly 166 29

Elton 89 Wilson 784 31 Wilson 781 32 Bonney 74 33 Wilson 783 34 Ibid.

35 Ibid.

36 Wilson 787 30

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peoples of Europe, who had absolutely no control over where the armies might head next, war could only bring even more strife and uncertainty.

As a whole the period thus marked a new height of instability in all facets of life— physical, intellectual, and spiritual. During the initial ravages of the Black Death in the early 1300s, people were too frightened of death to turn away from the Church; on the contrary, the Church was the only truly stable institution to which Europeans could cling. Now, however, faced by war, starvation, and death, there no longer existed such a bastion of strength. The Reformation had reopened the question of religious individuality and dissent, thus permanently destroying the former stabilizing monolithic authority of the single Church. Meanwhile, the Scientific Revolution threatened the shared religious worldview of all Christians, cutting at the very core of the system to which people had subscribed since their birth, the only worldview they had ever known. Meanwhile, wars raged across the continent in which thousands (and sometimes millions) died and which brought the average person only more misery. The involvement of religion in such conflicts intensified the brutality and removed what safety one might have had in their chosen beliefs. The result was “general anxiety at the loss of stability.”37 In such a climate of insecurity and confusion, people sought to gain control over what little aspects of their lives they could.

The best tried-and-true method of doing so was through scapegoating. “Majority cultures have frequently ascribed responsibility for social disaster”38 on scapegoats, foisting their problems and fears onto a group which can then be easily punished for the many misfortunes undergone. Europe was no exception, as it had a fine history of doing so, mostly to the Jews.

During the sixteenth and seventeenth centuries, witches became the scapegoat for all the distress and upheaval Europeans at all levels of society had undergone. “It was no accident that the great witchcraft hysteria, one of the most distinctive phenomenon in the age of religious wars, began in the 1560s;”39 by 1560, the combination of the religious, political, and scientific turmoil reached the point where people began subconsciously scapegoating in order to regain at least the semblance of control over their lives. Europeans “had a desperate need for scapegoats to meliorate the impact of social disasters for which they had no remedy,”40 and witches filled the role admirably indeed.

Scapegoating is purely reactionary; it does no actual good, and once started it is difficult to stop. What makes it so appealing, however, is that it appears to those doing it to be the exact opposite—it is instigated by one’s self, so it seems active rather than reactive; the ability to destroy one’s target makes it seem incredibly beneficial; and when one truly believes in one’s actions, of course one can stop, but only when the perceived threat has been completely silenced.

All this was true of the witch-hunts. Massively intensifying in the 1560s as religious strife became intertwined with physical conflict and politics, the witch-hunts served to alleviate the fears of many by providing them something to do that at least seemed useful. Hunting witches allowed people to act instead of react. It let them take out all their frustrations on someone else without any personal guilt or fear of repercussions. There was absolutely nothing the average peasant could do about the movement of local armies, but there was absolutely nothing a city dweller or a local bishop could do about such things, either. As a result, “the course of the witch craze reflected the dominant political realities of the sixteenth and

37 Wilson 809 38 Klaits 17 39 40

Dunn 9 Ibid.

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seventeenth centuries.”41 In the search for a new spiritual identity while war raged round and science demolished old certainties, it was only natural that there would be failures as well as successes, and “the markers of such crises of identity are depression, despair, hate, resignation, and the quest for the scapegoat.”42 The immense social upheaval left the majority of people of all social classes helpless and afraid, and all they could do to assuage their fears was to manifest them in a scapegoat. The result was the devastating witch-hunts.

The usual European scapegoat was the Jewish community, the ultimate outsiders in terms of cultural and religious stereotype. However, unlike the continent’s past and future scapegoating crazes, the witch hunts resulted not from one particular massive crisis but from the more insidious insecurity created by the political and religious atmosphere of the times. Individual witch-hunts were often unconnected with each other, and each village’s craze came at a different time. “Witch hunts reflected ... the stresses in the daily lives of ordinary people,”43 so depending on when and where crisis hit, one village’s craze came far later than another’s.

Witches were wholly dismissed by the Church as pagan superstition until the twelfth century, and the modern image of the witch—the image so widely propagated during the witch hunts—did not fully come into being until the Renaissance and its fascination with mysticism as an alternative to the established Church. It was the dark side of the Reformation, partnered with the growing apocalyptic beliefs of many, that gave rise to the belief of witches as instruments of and partners with the Devil himself.

As the Reformation slowed down and began to meet real organized Catholic resistance during the second half of the sixteenth century, Reformers began to lose their optimism. To make up for their perceived growing inability to spread the true Word, “pessimism began to set in,”44 and one of the ways to counter this was to attack any religious deviancy with a new vigor and ferocity. Catholics, facing the similar problem of having to ensure true permanency for their religion, adopted these tactics as well in an attempt to root out any and all unorthodoxy. In addition, the apocalyptic views shared by Catholics and Protestants alike began to falter as people began to realize that the Second Coming was not quite so close at hand. “Recent analysis of apocalyptic ... expectations suggest that when an expected transformation fails to transpire, ... there is a tendency ... to project onto the opponent the blame for the collapse of one’s dreams.”45 Here, such believers felt that their disappointment was due to continued impurities within their own communities, and as a result they jumped at the chance to purify themselves further by chasing out those perceived to not be model Christians.

Misogyny did play a role in the witch-hunts, but it was not the main impetus by far. On average a good 25% of the witches killed were men.46 Preexisting sexism played out more in punishments (searches of accused females that had definite sexual overtones) than in the hunts themselves; the quest to eliminate religious deviancy affected women more partly because “ideologues strengthened the calls for patriarchalism”47 but mostly because there were simply more women available. Accused witches were often old and lived by themselves, and since “the

41 Klaits 131 42 Matheson 77 43 Klaits 92 44 Matheson 138 45 Matheson 83 46 Waite 7 47 Waite 117

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proportion of single women was growing at the time of the trials,”48 there were simply less old men around to come under suspicion.

Witches really were the perfect scapegoat. It was easy for “Catholic and Protestant polemics [to link] religious heresy to a demonic conspiracy,”49 and after the radicalization of Christianity prompted by the Reformation, elites were ready to believe in such plots. As a result, people on all levels of society were willing to scapegoat witches in order to properly cleanse their communities and demonstrate that they themselves were good Christians. The pursuit of witches often became part of the greater pursuit of religious orthodoxy, so “in several regions, witchcraft trials began just as heresy trials against Protestants and Anabaptists ended.” Religious, political, and social uncertainty provided the impetus for the hunts, but religious extremism provided the target.

48 Klaits 95

49 Waite 116

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Hunt for the Heretic Conclusion

The European witch-hunts of the sixteenth and seventeenth were the result of not just social upheaval but the accompanying religious extremism and drive for religious orthodoxy.

Ironically, the Reformation, which had spawned one of the greatest outpourings of religious diversity, now launched a conservative movement. In response to the growing radicalization of the Reformation and social instability caused in part by religious sentiment as well, Catholics and Protestants reacted by attacking heresy (whether real or perceived) and any threats to doctrinal unity within individual communities.

After the initial spread of the Reformation, the spread of Protestantism slowed dramatically, and in some places the Catholics actually regained territory. Religious competition meant that both groups grew more paranoid about the strength and staying power of their faiths; the only way to ensure the continuation of a religion, both sides felt, was to eliminate any departures from strict doctrine. This conservatism played a large role in the attacks on heretics directly preceding the witch-hunts.

As Waite points out, in many regions the witch-hunts began when the heretic trials were ending, implying continuity between the two. When communities ran out of actual heretics to hunt but still felt just as dissatisfied religiously, diabolical-conspiracy theories probably rose in popularity. The simultaneous social instability caused by the Scientific Revolution and the religious wars spreading across the continent made the need for a scapegoat tantamount, and the earlier fears about heretics and the Second Coming provoked people into searching for a scapegoat that could be directly linked to Satan. The Renaissance myth of the witch as practitioner of black magic and ally to the Devil provided a target that matched both the social and religious scapegoating needs. The witch-hunts were the direct result of this social and religious upheaval.

17

Hunt for the Heretic Bibliography

Barstow, Anne Llewellyn. (1994.) Witchcraze: A New History of the European Witch Hunts. San Francisco: Pandora.

Bonelli, Righini and William R. Shea (Eds.). (1975.) Reason, Experiment, and Mysticism. New York: Science History Publications.

Bonney, Richard. (2002.) Essential Histories: The Thirty Years’ War, 1618-1648. Oxford: Osprey.

Cole, Richard G. (1972.) “The Dynamics of Printing in the Sixteenth Century.” From The Social History of the Reformation, ed. Lawrence P. Buck and Jonathan W. Zophy. Columbus: Ohio State University. 93-105.

Dunn, Richard S. (1970.) The Age of Religious Wars, 1559-1715. 2nd Edition. New York: Norton.

Elton, G.R. (1963.) Reformation Europe: 1517-1559. London: Fontana Press.

Gerard, J. (1909). Galileo Galilei. In The Catholic Encyclopedia. New York: Robert Appleton Company. Retrieved June 1, 2012 from New Advent: http://www.newadvent.org/cathen/06342b.htm.

Hannam, James. (2011.) The Genesis of Science: How the Christian Middle Ages Launched the Scientific Revolution. Washington, D.C.: Regnery Publishing.

Jensen, De Lamar. (1981.) Renaissance Europe: Age of Recovery and Reconciliation. Lexington, MA: D.C. Heath and Company. 191-218.

Kidd, B.J. (1933.) The Counter-Reformation, 1550-1600. London: Society for Promoting Christian Knowledge.

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Kirsch, J.P. (1911). The Reformation. In The Catholic Encyclopedia. New York: Robert Appleton Company. Retrieved June 1, 2012 from New Advent: http://www.newadvent.org/cathen/12700b.htm.

Klaits, Joseph. (1985.) Servants of Satan: The Age of the Witch Hunts. Bloomington: Indiana University.

Matheson, Peter. (2001.) The Imaginative World of the Reformation. Minneapolis: Fortress Press.

Oâ&#x20AC;&#x2122;Connell, Marvin R. (1974.) The Counter Reformation: 1559-1610. New York: Harper & Row. Spahn, M. (1912). The Thirty Years War. In The Catholic Encyclopedia. New York: Robert Appleton Company. Retrieved June 1, 2012 from New Advent: http://www.newadvent.org/cathen/14648b.htm.

Mattingly, Garrett. (1955.) Renaissance Diplomacy. New York: Dover Publishing.

Rice, Eugene F. Jr. and Anthony Grafton. (1970.) The Foundations of Early Modern Europe, 1460-1559. 2nd Edition. New York: Norton.

Waite, Gary K. (2003.) Heresy, Magic, and Witchcraft in Early Modern Europe. New York: Palgrave Macmillan.

Wilson, Peter H. (2009.) The Thirty Years War: Europeâ&#x20AC;&#x2122;s Tragedy. Cambridge: Belknap Press.

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Consider the Jellyfish: Understanding the Process of Ageing and Death

by Angela Niu, ‘12 Abstract Birth, maturation, reproduction, age, illness, and death are the six major events of all living organisms. Ageing and death in our minds are the also sections of the ecosystem.

However, many simple and primitive organisms such as Sanicula and Spongiatia can also achieve longevity. Even more strikingly, a species of jellyfish, Turritopsis nutricula, can avoid death by rejuvenating endlessly and therefore achieve “immortality” theoretically unless they are ill or killed. Moreover, inestimable numbers of marine species remain undiscovered in the mysterious ocean. These facts have lead scientists to question the existence of life cycles, to explore the secret of ageing, and to do research on cellular and molecular levels. Two types of cells, the stem cells and cancer cells, are very much related to the understandings of ageing and death. In Part I of this paper, I will introduce the existing results of scientific research about the causes of ageing and death and relative concepts of stem cells and cancer cells. In Part II, I will utilize real life examples to further explain and understand the process of ageing and death.

PART I: Introduction To The Biochemistry Of Ageing 1.1 Ageing Theories There are various theories explaining the causes of ageing, each from a different viewpoint. At present, the ageing theories are classified into three categories: biological theories, genetic theories, and non-biological theories. The biological theories see the ageing process as a result of evolution and body cycle in controlled manners; that is, the ageing and death of organisms are designed and programmed because they are naturally favorable. However, the ultimate biological basis of aging remains unknown. The genetic theories attribute cell ageing and death to the accumulation of damage to the genes, or DNA, by either internal or external facts. The genetic field is therefore highly favored by the modern scientific world. Non-biological theories are not science related. Instead, they attribute ageing (especially of the elderly) to spiritual facts, such as their degree satisfaction with life and their religious attributes. In this paper, the biological theories of ageing are my primary concern. The following sections 1.2-1.5 provide the background information for Part II, so if you are aware of the concepts of telomeres, cellular differentiation, stem cells, and cancer cells, please feel free to jump to 1.6, “Relating Ageing to stem and cancer cells.”

1.2 Telomere One of the many biological theories of ageing is the Telomere Theory.

Telomeres are the structures at the end of chromosomes; they only exist in eukaryotic cells. In contrast to the genes that are the blueprints of functional polypeptides, or

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proteins, telomere are composed of non-coding nucleic acids that aim to protect the chromosomes from deterioration or from fusion with another chromosome. Each eukaryotic cell division involves the duplication of DNA; the replicated DNA strand is shorter than the template DNA strand due to the incomplete semiconservative DNA replication.

Therefore, the telomeres, which are located at the end of DNA strands in eukaryotic cells, are consumed in each cell division.

In somatic cells and differentiated cells of eukaryotes, such shortening of telomeres are not replenished because these cells lack active telomerase, an enzyme that replenishes the shortened telomeres by adding nucleic acids after each cell division. Hence, a cell dies or loses the capability of division after certain times of cell division in eukaryotes. Therefore, telomere shortening is considered to contribute to cell ageing and death in the cellular level in eukaryotes; this is the core idea of the Telomere Theory.

In contrast to eukaryotic somatic cells, eukaryotic stem cells, germ cells, and hair follicles have active telomerase and thus are capable of self-renewal. One example of the difference between eukaryotic somatic cells and germ cells is Dolly the Sheep. In this historical event of cloning technology, the resulting cloned sheep Dolly had poor cellular vitality and health. In fact, Dolly had the same cellular age with the sheep that was the DNA donor; she was old even though she was a newborn. The reason lay in the fact that the genetic materials in the mammary cells of the donor had shortened telomeres, which then gave Dolly aged cells. In contrast, Normal embryos develop from germ cells that have complete telomeres so that normal babies have young cells.

Prokarotes lack telomeres, so how can prokaryotes divide infinitely? The answer lies in the shape of prokaryotic DNA strands. Unlike eukaryotic DNA strands, which need telomere caps to prevent the fusion of the heads and ends, the prokaryotic DNA is circular, having the head and end of DNA strands joined together.

Therefore, prokaryotes do not need telomeres to keep DNA strands separate. On the other hand, prokaryotes do not have complicated genetic systems that need to be kept separate, such as homologous pairs and the condensation to

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chromosomes that are only present in eukaryotes. Furthermore, because of the circular shape of DNA, prokaryotic DNA replication is complete without any loss of nucleic acids and the shortening of DNA. In this paper, we are only concerned with eukaryotic cells.

1.3 Cellular Differentiation Undifferentiated, differentiated, ageing, and death are the four steps that an embryonic cell can go in a eukaryote. Why are skin cells and muscle cells different?

How do we have different types of cells?

The functions and appearances of a cell are all determined by the proteins that it produces. For example, hair follicles produce protein keratin, which is the primary component of hair, while muscle cells produce the proteins actin and myosin, which form the sarcomeres and enable motor contraction. Even though these cells are different, they all have the same genome, or the same set of DNA. So how do cells know which proteins to produce?

During embryonic development, growth factors from the cytoplasm of the zygote (also called cytoplasmic determinants) determine cell fates by regulating gene expression of the cells. As the growth factors turn on and off genes of a cell, the cell become differentiated, or specialized.

The original, undifferentiated cells are stem cells, which are capable of differentiating into any type of cell with certain growth factors. Growth factors can regulate gene expression by signaling the cell to wrap or unwrap chromatins (which can be achieved by either DNA methylation or histone acetylation), to turn on or off transcription factors, such as promoters, enhancers, operators, etc. Some operations or modifications in DNA are irreversible; cells with irreversible DNA modifications are fully differentiated. A muscle cell is one example of a fully differentiated cell. However, most operations are reversible; such reversibility is important to the integrity and internal regulation of organisms. Internal

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regulations can be achieved by hormones, which are regulated by the endocrine system, in adulthood.

1.4 Stem Cells Asexual reproductive organisms can divide infinitely; therefore, they never age or die. But since these organisms usually split, it is hardly known if they have awareness as complex animals do. However, almost all complex animals are mortal, each species restricted to its life-span, which is determined by the average time of cell divisions of important organs among its individuals. In agriculture, to avoid disadvantageous crossbreeding, plants are asexually reproduced from a piece of stem or root. However, we can hardly imagine mammals or birds to reproduce in this way. Such a difference leads to the case of stem cells.

Stem cells are undifferentiated cells that are capable of self-renewal and differentiating into other types of cells in multi-cellular organisms.

As introduced in the early sections of “Telomere” and “Cell Differentiation,” stems cells are capable of self-renewal because they have telomerase to replenish telomeres; they are undifferentiated so they can develop into other types of cells.

Stem cells can be totipotent (capable of differentiating into all cells of one organism), pluripotent (capable of differentiating into nearly all cells of one organism), multipotent (capable of differentiate into a number of cells in one tissue), oligopotent (capable of differentiate into only a few closely related cells), or unipotent (can renew only the cell itself). In mammals, totipotent stem cells only exist in morula, which is a zygote after several divisions. Embryonic stem cells are pluripotent; they are undifferentiated cells forming the Inner Cell Mass of blastocyst, which is the following stage of morula. Pluripotent stem cells are very rare in adults and children, but can be found in a number of tissues including umbilical cord blood, which are critical in medical research. Tissue stem cells are multipotent; they live in body’s tissues and are capable of differentiating into cells only in that particular tissue. Progenitor cells are oligopotent. Lymphoid progenitors and myeloid progenitors can mature into various immune cells and blood cells. Unipotent stem cells have lost the property of differentiation; they are different from fully different cells only because they are capable of self-renewal. One example of unipotent stem cells is liver cells, which can regenerate themselves when needed.

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In modern stem cell research, human embryonic stem cells can be extracted from donated blastocyst. These pluripotent stem cells are then grown in cultures that have certain growth factors, which then lead to the formation of organs for medical utilization. However, human embryonic stem cell utilization is highly controversial in society, so another focus of stem cell research is to reprogram multipotent stem cells into pluripotent stem cells. At present, pluripotent reprogramming has encountered many difficulties because many reprogramming factors are not discovered. Another method is transdifferentiation, or lineage reprogramming, a process in which a mature somatic cell is transformed into another type of somatic cell without undergoing stem cell state; this is more practical.

Plant stem cells are pluripotent, which means that any segment of plant that contains enough stem cells can generate a new plant.

Meristematic cells, or plant stem cells, are located in the plant tissue meristem. Plant structure is also critical in vegetative propagation, or plant cloning because a plant has meristem all over its body. However, in artificial vegetative propagation, or horticulture, only shoots and roots of donor plants are used because apical meristematic cells, which only locate in the shoot or shoots, are nearly completely undifferentiated. Apical meristem also exists on plant stems where branches initiate, which are called nodes.

Types of shoots and roots that are capable of vegetative propagation involve stems, basal shoots, tubers, rhizomes, stolons, corms, bulbs, and buds. Even leaves can be used for plant cloning when they are treated with appropriate nutrition and hormones.

Besides plants, many simple animals are capable of asexual reproduction despite the fact that they normally produce sexually. Starfish, planarian, earthworms, and sponge animals are capable of regenerating their lost body parts when cut. A planarian split into two parts can regenerate into two genetically identical individuals. These animalsâ&#x20AC;&#x2122; interesting ability to regenerate is also given by stem cells.

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1.5 Cancer Cells Cancer cells are characterized by unregulated growth and the invasion and spread of cancer cells from a primary site to secondary sites, or other parts of the body. Cancer is a genetic disease in the cellular level. Mutations on the genetic materials of cells occur all the time. Special enzymes in cells proofread and repair DNA sequences to ensure that the DNA is free of mutations, but accidents that lead to disrepair of DNA can pass the mutations on to the offspring of a mutated cell. Not all mutations can lead to cancerâ&#x20AC;&#x201D; only mutations of proto-oncogenes, genes that regulate cell proliferation and death, can cause the initiation of tumors. Two specific examples of protooncogenes are the growth inducing gene and the tumor suppressor gene. The former gene, once mutated, leads to unregulated cell proliferation. The latter gene is critical in the apoptosis response, or programmed cell death once unregulated cell proliferation is detected.

Carcinogenesis, the process in which a normal cell develops into a cancer cell, is a function of natural selection.

Both the growth inducing gene and tumor suppressor gene must be mutated in order for a cancer cell to develop. Since mutated cells are constantly under the attack of the immune system, mutated cells that are unable to develop into robust cancer cells diminish. Thus, under natural selection, the surviving cancer cells have the properties to proliferate rapidly, to escape programmed cell death, and to divide infinitely.

Natural selected cancer cells must also have their telomeres replenished so they can divide infinitely because DNA would degrade without the protection of telomeres. Most cancer cells have telomeres that are activated, while others use the Alternative Lengthening of Telomeres (ALT) pathway to replenish their telomeres.

The risk of carcinogenesis increases with age in mammals because mutation rates increase with time and numbers of cell division. Thus, limited length of telomere in a cell is critical in preventing carcinogenesis because limited times of cell division means smaller possibility of mutation.

Figure 9: Cancer staging

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Another vital hallmark of cancer cells is metastasis, the spread of cancer cells to other parts of the body. Metastasis is the property that makes cancer a lethal disease.

Benign tumors can be surgically removed; malignant tumors, however, can never be efficiently removed. “Hook” proteins are important in cell-to-cell communication and adhesion so tissue layers stick together to function properly as a whole. Genes that code for “hook” proteins, such as the E-cadherin gene, are indispensible in securing cell-tocell adhesion and therefore in keeping a benign tumor from transforming into a malignant tumor. However, once these “hook” genes mutate and no longer function, cancer cells are free to detach from the tumor and migrate. In order for cancer cells to achieve intravasation (the penetration of cancer cells into blood or lymphatic vessels), transport (the transport of cancer cells to other parts of body through blood and lymphatic vessels), extravasation (the escape of cancer cells from blood or lymphatic vessels), and metastatic colonization (the colonization and proliferation of migrating cancer cells in second sites), the gene coding for integrins and the gene coding for proteases must also mutate.

Mutation of integrins provides cancer cells motility while mutation of proteases enables cancer cells to eat up the base membrane blood vessels. At present, even though carcinogenesis and metastasis are well understood, many mutated genes have not been discovered yet.

1.6 Relating Ageing to stem and cancer cells Have you ever seen an old starfish or hydra? A few selected animals exhibit negligible senescence, or the lack of symptoms of aging. Having the properties of selfrenewal and infinite division, stem cell is the origin of cell vitality and organism longevity; it hence contributes to negligible senescence. Many primitive plants and simple animals, if are taken great care of, can achieve immortality theoretically. The oldest known clonal plant species Populus tremuloides is at least 80,000 years old, and it will continue to age. The oldest known ground plant is a Great Basin Bristlecone Pine, which is 4,842 years old. The oldest known animal, the black coral, is around 4,265 years old. Three common factors of these longest-living and even immortal organisms are that they are simple, they have plenty stem cells, and there are few of them. And these two factors explain why complex organisms are all mortal: complex organisms can hardly keep all of their somatic systems to function in balance all the time; complex organisms do not have many stem cells; the evolutionary advantage of complex organisms are not to live long but to pass their genetic materials to offspring in order to adapt to the constantly changing environment.

It is inevitable that stem cells are related to ageing and mortality, but what is the role of cancer? Cancer is a disease that complex organisms never expect. Humans have evolved hard to lower the possibility of the emergence of cancer cells. In the human genome, there are 20 tumor suppressor genes that have been discovered. Scientists are still working hard to figure out what the other tumor suppressor genes are. There are even various metastasis suppressor genes in our DNA chains so our body can keep benign tumor from transforming into malignant tumor as long as possible. As stated in the previous section 1.5, “the risk of carcinogenesis increases with age in mammals because mutation rates increase with time and numbers of cell division,” so we can assume that

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mortality is programmed in our genes in order to minimize carcinogenesis. According to the Telomere Ageing Theory, the limited length of telomere and lack of telomerase in the somatic cells of complex organisms set the clock for life spans. Therefore, telomere is the factor that programs our death. Whatâ&#x20AC;&#x2122;s more, looking at the chart below, one might ask why the cancer rates decreases from 75-85+ years old. There are many factors that contribute to this phenomenon. People who survive over 74 years old usually live healthy lives, which mean lower exposure to carcinogens. These healthy old people are also the consequence of natural selection because people who are less healthy, who are more exposed to carcinogens, and who have a higher chance of genetic mutations, die, leaving the surviving population relatively healthy. However, even though cancer rates decreases from 75 years old, the cancer rates are still high relative to young children and adults.

Figure 1: Cancer rates by age group

However, there is no single answer to the causes of aging and mortality. Other genetic mutations and DNA damage that are not as malignant as cancer also contribute to malfunction or loss of function of proteins. According to several genetic ageing theories, the amount of genetic mutations increases steadily, with time, ageing and death as the results of non-functional genes and proteins. For example, loss of hearing, vision, memory, immune response, and motility are common in the elderly population. The incidence of genetic diseases also increases with time. These disadvantages of genetic mutations and damage certainly do not benefit natural selection; hence mortality rates increase as age increases. Furthermore, according to the data below, the population of 35-

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44-year-olds forms a significant contrast with the population of 85+-year-olds. Such difference in population means that most people die of diseases or accidents before they get old enough to die naturally. Thus, low genetic mutation rates, which are determined by good health conditions and young age, are naturally selected and evolutionarily advantageous.

Figure 2: Population by age group.

PART II: Examples And Further Exploration 2.1 Turritopsis nutricula This strikingly beautiful animal, originating in the Pacific but now spread all over the worldâ&#x20AC;&#x2122;s oceans, has one of the oddest fates among all of the living beings on Earth. As mentioned in the abstract of this paper, the immortal jellyfish Turritopsis nutricula has the ability of legendary phoenix: rejuvenating themselves endlessly every time they become sexually mature and reproduce. Turritopsis nutricula is the only known species with such rejuvenating ability to escape death. Since this species is immortal, the population is rising fast and invading the ocean.

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Differing from the species with negligible senescence, Turritopsis nutricula does mature before it transforms back into its polyp stage, or immature stage. Scientists have agreed that the species rejuvenate through transdifferentiation, when the jellyfish “alters the differentiated state of the cell and transform it into a new cell.” This process of transdifferentiate requires the certain cell types, including tissues from both the jellyfish’s bell surface and is circulatory canal.” However, without enough laboratory experimentation, the science of Turritopsis nutricula is not fully understood at present.

Turritopsis nutricula raised in laboratory has shown an immortality rate of 100%, but in nature, Turritopsis nutricula always die as a result of being eaten as plankton or of diseases.

2.2 Do invertebrates, such as planarian and starfish, have cancer?

Based on the conditions that carcinogenesis requires, the answer for this question is yes. In fact, cancer cells can emerge from any cell type, including stem cells. So there is little wonder that organisms that have a lot of stem cells can have cancer.

Cancer stem cells are cancer cells that possess characteristics associated with normal stem cells.

Cancer stem cells can derive from mutated stem cells and have the ability to give rise to several different types of Figure 3: Stem cell specific and conventional cancer cancer cells that are not cancer stem therapies. cells in one tumor. These derived cancer cells are usually not capable of mitosis, or cell division. Tumors that are originated with cancer stem cells are more likely to become malignant and to go through the metastasis stages. However, even these tumors are more likely to spread and are therefore more lethal than conventional tumors; they are somewhat easier to treat, though, because cancer stem cells have proteins that normal cancer cells do not have. Cancer stem cells’ specific therapy targets and kills cancer stem cells by inhibiting the function of these special proteins. Then those cancer cells derived from cancer stem cells die out naturally because they do not divide.

Since cancer cells are immortal and can keep growing as long as there is enough nutrition, one might wonder if these cancer stem cells can transform a planarian, whose cells are almost all stem cells, into a whole new creature that has all of is stem cells replaced by cancer stem cells. The answer is no. Note that the basis of carcinogenesis is

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genetic mutation, or mutations of DNA sequences. And DNA is the blue print of proteins that are the building and functional blocks of cells. So what genetic mutations result in are the nonfunctional or malfunctioned proteins, which then lead to malfunctioned cells.

Under normal circumstances, nonfunctional or malfunctioned cells trigger apoptosis, voluntary cell suicide coded by tumor suppressor genes, or the attack of the immune system. However, the facts that cancer cells are incapable of apoptosis and that invertebrates, such as planarians, do not have strong immune systems have made cancer extremely dangerous and lethal to invertebrates.

2.3 Does longer telomere mean longer life span?

Leonard Hayflick first discovered the phenomenon of limited cellular division of somatic cells; he named this phenomenon the Hayflick limit. Professor Elizabeth Blackburn at the University of California, San Francisco has done experimentation on telomere extension in order to extend the Hayflick limit and therefore to find means of human life extension. Blackburn conducted experiments in which telomeres of mice were lengthened by using drugs that could temporarily turn on telomerase or by using gene therapy. The result was successful and fascinating: a number of laboratory mice have shown revered signs of aging. The same results come out after the experiment was performed on the nematode worm species Caenorhabditis elegans. Thus, even though the results are not proven in humans, telomere extension does support the Telomere Ageing Theory and provides means renewable organ tissues for medical utilization and even means of human life extension.

However, the role of telomeres is still far from being fully understood because lengthened telomeres are hypothesized to increase the chance of cancer. On the other hand, long telomeres might also protect against cancer because short telomeres are associated with cancer cells and carcinogenesis.

Furthermore, the odd behaviors of the telomeres of two long-lived seabird species have suggested that telomeres are far more complicated than scientists have long believed. In 2003, scientists observed that the telomeres of Leachâ&#x20AC;&#x2122;s Storm-petrel, Oceanodroma leucorhoa, lengthened with chronological age. While in 2006, Juola et al. reported that the telomeres of another unrelated seabird species the Great Frigatebird, Fregata minor, decreased until at least chronological 40 years of age, even over the entire life span. Even more odd was that the speed of telomere consumption slowed down massively with increasing age and the speed of telomere shortening varied greatly within the individuals of the same population.

Figure 4: Leachâ&#x20AC;&#x2122;s Storm Petral

Figure 5: Great Frigatebird

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PART III: Conclusion The paper has disclosed the known biological and genetic causes of ageing and mortality. We now know that life extension through technology is very possibly applicable in the future. Even though the secret of ageing and mortality has not been fully understood yet, scientists are making progress all the time. Life is fascinating; it is the crystallization of time, chemistry, physics, and even the universe. As we progress toward decoding the secrets of life through scientific means, we should not forget to appreciate and respect it.

Reference Ageing, Wikipedia, http://en.wikipedia.org/wiki/Ageing#Theories Cancer, Wikipedia, http://en.wikipedia.org/wiki/Cancer Cancer Staging, Wikipedia, http://en.wikipedia.org/wiki/Cancer_staging Cancer Stem cell, Wikipedia, http://en.wikipedia.org/wiki/Cancer_stem_cell Cellular differentiation, Wikipedia, http://en.wikipedia.org/wiki/Cellular_differentiation Cloning, Wikipedia, http://en.wikipedia.org/wiki/Cloning List of long-living organisms, Wikipedia, http://en.wikipedia.org/wiki/List_of_longliving_organisms Mueller, Laurence D., Casandra L. Rauser, and Michael R. Rose. Does Aging Stop? New York: Oxford UP, 2011. Print.

Negligible senescence, Wikipedia, http://en.wikipedia.org/wiki/Negligible_senescence Neoplastic transformation in the planarian: II. Ultrastructure of malignant reticuloma, Wiley Online Library, http://onlinelibrary.wiley.com/doi/10.1002/jez.1402400210/abstract Pecorino, Lauren. Molecular Biology of Cancer: Mechanisms, Targets, and Therapeutics.

2nd ed. Oxford: Oxford UP, 2008. Print.

Planarian, Wikipedia, http://en.wikipedia.org/wiki/Planarian Prokaryotic DNA replication, Wikipedia, http://en.wikipedia.org/wiki/Prokaryotic_DNA_replication Schneider, Meg F. Stem Cells for Dummies. Hoboken, NJ: Wiley, 2010. Print.

Stem cell, Wikipedia, http://en.wikipedia.org/wiki/Stem_cell

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Telomere, Wikipedia, http://en.wikipedia.org/wiki/Telomere#References Turritopsis nutricula, Wikipedia, http://en.wikipedia.org/wiki/Turritopsis_nutricula Vegetative reproduction, Wikipedia, http://en.wikipedia.org/wiki/Vegetative_reproduction Images Cited Figure 1: http://en.wikipedia.org/wiki/File:Telomere_caps.gif, 2008-01-28 20:46 (Original text : http://science.nasa.gov/headlines/y2006/images/telomeres/caps_med.jpg) Figure 2: http://en.wikipedia.org/wiki/File:Dolly_clone.svg, 2008-04-12 12:58 Figure 4: http://en.wikipedia.org/wiki/File:Stem_cell_division_and_differentiation.svg, 2007-05-15 21:13 Figure 5: http://en.wikipedia.org/wiki/File:Stem_cells_diagram.png, 2009-03-25 11:57 Figure 6: Freudenrich, Ph.D., Craig. "How Cloning Works" 26 March 2001. HowStuffWorks.com. <http://science.howstuffworks.com/environmental/life/genetic/cloning.htm> 24 May 2012.

Figure 8: http://en.wikipedia.org/wiki/File:Cancer_requires_multiple_mutations_from_NIHen.png, 2007-04-19 22:58 Figure 9: http://en.wikipedia.org/wiki/File:Cancer_stages.png, 2011-06-30 19:07 Figure 10: National Program of Cancer Registries: 1999 - 2009 Incidence, WONDER On-line Database. United States Department of Health and Human Services, Centers for Disease Control and Prevention and National Cancer Institute; 2011. Accessed at http://wonder.cdc.g Figure 11: Centers for Disease Control and Prevention, National Center for Health Statistics. Compressed Mortality File 1999-2008. CDC WONDER Online Database, compiled from Compressed Mortality File 1999-2008 Series 20 No. 2N, 2011. Accessed at http://wonder.cdc.go Figure 12: Swarms of Immortal Jellyfish, Betty the Butterflyâ&#x20AC;&#x2122;s Blog, a-z animals, http://a-z-animals.com/blog/swarms-of-immortal-jellyfish/

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Figure 13: http://en.wikipedia.org/wiki/File:Cancer_stem_cells_text_resized.svg, 200605-29 22:52 Figure 14: http://en.wikipedia.org/wiki/File:Polycelis_felina.jpg, 2011-01-31 20:27 Figure 15: http://en.wikipedia.org/wiki/File:Lesp1.jpg, 2006-06-17 08:35 Figure 16: http://en.wikipedia.org/wiki/File:Male_greater_frigate_bird_displaying.jpg, 2012-03-30 Glossary Actin: A globular protein that links into chains, two of which twist helically about each other, forming microfilaments in muscle and other contractile elements in cells.

Chromatin: The complex of DNA and proteins that makes up a eukaryotic chromosome.

When the cell is not dividing, chromatin exists as a mass of very long, thin fibers that are not visible with a light microscope.

Cytoplasm: The entire contents of the cell, exclusive of the nucleus, and bounded by the plasma membrane.

Cytoplasmic determinants: In animal development, substances deposited by the mother in the eggs she produces that regulate the expression of genes affecting the early development of the embryo.

DNA methylation: The addition of methyl groups (â&#x20AC;&#x201C;CH3) to bases of DNA after DNA synthesis; may serve as a long-term control of gene expression.

Endocrine system: The internal system of chemical communication involving hormones, the ductless glands that secrete hormones, and the molecular receptors on or in target cells that respond to hormones; functions in concert with the nervous system to effect internal regulation and maintain homeostasis.

Eukaryotes: An organism whose cells contain membraine-bound organelles and whose DNA is enclosed in a cell nucleus and is associated with proteins.

Histone: A small protein with a high proportion of positively charged amino acids that binds to the negatively charged DNA and plays a key role in its chromatin structure.

Histone acetylation and deacetylation: In histone acetylation and deacetylation, the histones are acetylated and deacetylated on lysine residues in the N-terminal tail and on the surface of the nucleosome core as part of gene regulation. These reactions are typically catalyzed by enzymes with "histone acetyltransferase" (HAT) or "histone deacetylase" (HDAC) activity. The source of the acetyl group in histone acetylation is Acetyl-Coenzyme A, and in histone deacetylation the acetyl group is transferred to Coenzyme A. Integrin: Receptors that mediate the attachment between a cell and the tissues that surround it, such as other cells or the extracellular matrix (ECM). In signal transduction, integrins pass information about the chemical composition of the ECM into the cell.

Therefore, they are involved in cell signaling and the regulation of cell cycle, shape, and motility.

Keratin: One of a group of tough, fibrous proteins formed by certain epidermal tissues and especially abundant in skin, claws, hair, feathers, and hooves.

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Meristem: Plant tissue that remains embryonic as long as the plant lives, allowing for indeterminate growth.

Mitosis: A process of nuclear division in eukaryotic cells conventionally divided into five stages: prophase, prometaphase, metaphase, anaphase, and telophase. Mitosis conserves chromosome number by equally allocating replicated chromosomes to each of the daughter nuclei.

Myosin: A type of protein filament that interacts with actin filaments to cause cell contraction.

Nucleic acid: A polymer consisting of many nucleotide monomers; serves as a blueprint for proteins and, through the actions of proteins, for all cellular activities. The two types are DNA and RNA. Prokaryotes: A group of organisms that lack a cell nucleus (= karyon), or any other membrane-bound organelles.

Protease: Any enzyme that conducts proteolysis, that is, begins protein catabolism by hydrolysis of the peptide bonds that link amino acids together in the polypeptide chain forming the protein.

Rhizome: In vascular plants, a horizontal stem growing along or below the surface of the soil; may be enlarged for storage or may function in vegetative reproduction.

Sarcomere: The fundamental, repeating unit of striated muscle, delimited by the Z lines.

Stolon: stolons (from Latin stolĹ? "branch") are horizontal connections between organisms. They may be part of the organism, or of its skeleton; typically, animal stolons are external skeletons.

Transcription: The synthesis of RNA on a DNA template.

Transcription factor: A regulatory protein that binds to DNA and stimulates transcription of specific genes.

All of the above definitions come from the sources below: Glossary of Biological terms, PHSchool, Pearson Education, http://www.phschool.com/science/biology_place/glossary/Wikipedia, en.wikipedia.org