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In small clinical studies in humans, epigenetic differences have been linked to differences in risk-taking and reactions to stress. Specifically, epigenetic differentiation in [[Twin#Monozygotic ("identical") twins|monozygotic twins]] has been shown to play a role in individual differences in:
In small clinical studies in humans, epigenetic differences have been linked to differences in risk-taking and reactions to stress. Specifically, epigenetic differentiation in [[Twin#Monozygotic ("identical") twins|monozygotic twins]] has been shown to play a role in individual differences in:
* risk-taking that is characterized by impulsive or disinhibited decision making.<ref name="Kaminsky_2008">{{cite journal | author = Kaminsky Z, Petronis A, Wang SC, Levine B, Ghaffar O, Floden D, Feinstein A | title = Epigenetics of personality traits: an illustrative study of identical twins discordant for risk-taking behavior | journal = Twin Res Hum Genet | volume = 11 | issue = 1 | pages = 1–11 | year = 2008 | month = February | pmid = 18251670 | doi = 10.1375/twin.11.1.1 | url =http://www.ncbi.nlm.nih.gov/pubmed/18251670 }}</ref>
* risk-taking that is characterized by impulsive or disinhibited decision making.<ref name="Kaminsky_2008">{{cite journal | author = Kaminsky Z, Petronis A, Wang SC, Levine B, Ghaffar O, Floden D, Feinstein A | title = Epigenetics of personality traits: an illustrative study of identical twins discordant for risk-taking behavior | journal = Twin Res Hum Genet | volume = 11 | issue = 1 | pages = 1–11 | year = 2008 | month = February | pmid = 18251670 | doi = 10.1375/twin.11.1.1 | url =http://www.ncbi.nlm.nih.gov/pubmed/18251670 }}</ref>
* the levels of [[anxiety]] and somatic complaints<ref name="Kaminsky_2008"/>
* the levels of [[anxiety]] (a state of apprehension or fear<ref name="pmid10235121">{{cite journal | author = Bakish D | title = The patient with comorbid depression and anxiety: the unmet need | journal = J Clin Psychiatry | volume = 60 Suppl 6 | issue = | pages = 20–4 | year = 1999 | pmid = 10235121 | doi = }}</ref> that arises during stress<ref name="Finan et al">{{cite book|last=Finan, P., Zautra, A., & Wershba, R.|title=In R. Contrada & A. Baum (Eds.) The handbook of stress science: Biology, psychology and health|year=2011|publisher=Springer Publishing Company|location=New York|isbn=9780826114716|pages=209–220|url=http://www.springerpub.com/Search/handbook%20of%20stress%20science}}</ref>) and somatic complaints<ref name="Kaminsky_2008"/> (physical ailments, symptoms and/or pain in the absence of underlying medical conditions).<ref name="isbn0-553-59226-2"/> Anxiety and somatic complaints have been associated with the broad personality trait of [[neuroticism]].<ref name="Costa and McRae, 1987">{{cite journal | author = Costa PT, McCrae RR | title = Neuroticism, somatic complaints, and disease: is the bark worse than the bite? | journal = J Pers | volume = 55 | issue = 2 | pages = 299–316 | year = 1987 | month = June | pmid = 3612472 | doi = }}</ref>


Epigenetic variations, associated with risk-taking behaviours and anxiety, have been linked to individual differences in lifestyle and career choices. In one study, each member of a pair of twins had chosen two very different life paths. One twin, who displayed high-risk behaviours (like gambling), chose a dangerous and high-sensation career as a war journalist. Despite the dangerous profession, this twin showed no elevated anxiety levels when confronted with stress. This twin married late in life (to an individual who also chose a dangerous profession), had no children, and consumed more alcohol than is considered medically healthy. In contrast, the other twin was considered to be a polar opposite. The second twin was prone to anxiety and developing somatic complaints when faced with stress.<ref name="Kaminsky_2008"/> Instead of displaying risk-taking behaviours, the second twin displayed risk-averse behaviours. The second twin chose a safe and predictable career as a manager in a law firm, married a lawyer, had children at a young age and had only traveled out of country once (to another English-speaking country).<ref name="Kaminsky_2008"/>
Epigenetic variations, associated with risk-taking behaviours and anxiety, have been linked to individual differences in lifestyle and career choices. In one study, each member of a pair of twins had chosen two very different life paths. One twin, who displayed high-risk behaviours (like gambling), chose a dangerous and high-sensation career as a war journalist. Despite the dangerous profession, this twin showed no elevated anxiety levels when confronted with stress. This twin married late in life (to an individual who also chose a dangerous profession), had no children, and consumed more alcohol than is considered medically healthy. In contrast, the other twin was considered to be a polar opposite. The second twin was prone to anxiety and developing somatic complaints when faced with stress.<ref name="Kaminsky_2008"/> Instead of displaying risk-taking behaviours, the second twin displayed risk-averse behaviours. The second twin chose a safe and predictable career as a manager in a law firm, married a lawyer, had children at a young age and had only traveled out of country once (to another English-speaking country).<ref name="Kaminsky_2008"/>

Revision as of 20:59, 7 December 2013

Epigenetics in psychology is an experimental science that seeks to explain how nurture shapes nature,[1] where nature refers to biological heredity[2] and nurture refers to virtually everything that occurs during the life-span (e.g., social-experience, diet and nutrition, and exposure to toxins).[1] Epigenetics in psychology attempts to provide a framework for understanding how the expression of genes is influenced by experiences and the environment[3] to produce individual differences in behaviour,[4] cognition[1] personality,[5] and mental health.[6][7]


Background

In biology, and specifically genetics, epigenetics is the study of heritable changes in gene activity which are not caused by changes in the DNA sequence; the term can also be used to describe the study of stable, long-term alterations in the transcriptional potential of a cell that are not necessarily heritable.[8][9]

Examples of mechanisms that produce such changes are DNA methylation[10] and histone modification[11], each of which alters how genes are expressed without altering the underlying DNA sequence. Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA.

Modifications of the epigenome do not alter DNA.

DNA methylation turns a gene "off" - it results in the inability of genetic information to be read from DNA; removing the methyl tag can turn the gene back "on".[12][13]

Epigenetics has a strong influence on the development of an organism and can alter the expression of individual traits.[14] Epigenetic changes occur not only in the developing fetus, but also in individuals throughout the human life-span.[15] Because epigenetic modifications can be passed from one generation to the next,[16] subsequent generations may be affected by the epigenetic changes that took place in the parents.[16]

Research into epigenetics in psychology

Anxiety and risk-taking

Monozygotic twins are identical twins. Twin studies help to reveal epigenetic differences related to various aspects of psychology.

In small clinical studies in humans, epigenetic differences have been linked to differences in risk-taking and reactions to stress. Specifically, epigenetic differentiation in monozygotic twins has been shown to play a role in individual differences in:

  • risk-taking that is characterized by impulsive or disinhibited decision making.[17]
  • the levels of anxiety and somatic complaints[17]

Epigenetic variations, associated with risk-taking behaviours and anxiety, have been linked to individual differences in lifestyle and career choices. In one study, each member of a pair of twins had chosen two very different life paths. One twin, who displayed high-risk behaviours (like gambling), chose a dangerous and high-sensation career as a war journalist. Despite the dangerous profession, this twin showed no elevated anxiety levels when confronted with stress. This twin married late in life (to an individual who also chose a dangerous profession), had no children, and consumed more alcohol than is considered medically healthy. In contrast, the other twin was considered to be a polar opposite. The second twin was prone to anxiety and developing somatic complaints when faced with stress.[17] Instead of displaying risk-taking behaviours, the second twin displayed risk-averse behaviours. The second twin chose a safe and predictable career as a manager in a law firm, married a lawyer, had children at a young age and had only traveled out of country once (to another English-speaking country).[17]

In this twin study, epigenetic differences in DNA methylation of the CpG islands proximal to the DLX1 gene have been implicated as affecting risk-taking behaviours and coping with stress in terms of anxiety.[17] DLX1 exerts its effects by helping to regulate the production of the neurotransmitter GABA (gamma-aminobutyric acid), and the hormone neuropeptide Y. GABA decreases stress[18] by acting on what is often referred to as the stress centre of the brain - the hypothalamic-pituitary-adrenal axis, or HPA axis.[19] Conversely, neuropeptide Y negates the effect of GABA on the HPA axis and results in an increased stress response.[20] Activation of the HPA axis, as part of the stress response, has been well-established in resulting in increased anxiety.[21] The epigenetic differences pertaining to GABA and neuropeptide Y, and their associated physiological HPA processes, have been posited to help explain individual differences in risk-taking behaviour and anxiety. In turn, this helps to explain why one twin functioned without anxiety under extremely dangerous situations.[17]

The researchers of the above twin study noted that despite the associations between epigenetic markers for individual differences in personality traits and behaviours that might influence occupational choices, epigenetics cannot on their own predict complex decision-making processes like career selection. Such complex decisions transcend genetic predication.[17]

Stress

The hypothalamic pituitary adrenal axis is involved in the human stress response.

The early parental care-giving environment has long been a central focus of human psychological development. Early abuse and neglect can lead to a wide range of cognitive and emotional impairments.[22] Animal studies reveal that the influence of early maternal care also affects genetic expression.[22] In their review of a series of studies, Szyf, McGowan and Meaney[23] indicated that early maternal care affected offspring's reactivity to stress. Specifically, the effects of maternal care in terms of the parental licking-grooming of offspring were examined. High licking-grooming resulted in a positive, long-term effect on the reactivity of the hypothalamic-pituitary-adrenal axis (HPA) as evidenced by decreased adrenocorticotropic hormone (ACTH) and corticosterone in response to stress in offspring. The effects of parental care on the HPA and ACTH resulted from epigenetic changes, whereby high licking-grooming led to decreased DNA methylation. In turn, decreased methylation allowed for increased access to the hippocampal glucocorticoid receptor genes in the offspring.[23] Increased expression of hippocampal glucocorticoid receptors causes the hippocampus to release less ACTH-releasing hormone, which acts on the pituitary gland to release less ACTH. In turn, a decrease in ACTH results in the adrenal glands releasing less cortisol. In contrast, less parental care (low licking-grooming) ultimately results in increased cortisol release.[22] The release of increased cortisol, via the HPA axis, as a reaction to psychological stress is well-established.[24][25] Therefore, pups that received less licking-grooming were more prone to react to stress.[22] Since humans also show the same cortisol response to stress and heritable cortisol levels,[26] the animal models have implications for humans.[23]

Research has demonstrated that the maternal genotype did not determine stress reactions in offspring. Instead, the early parental care environment affected genetic expression to influence how offspring react to stress. When rat offspring were removed from their low licking-grooming mothers and placed with high licking-grooming mothers, the epigenetic changes related to an increased stress response were reversed. The reverse was observed when pups were removed from their high licking-grooming parents and placed with low licking-grooming mothers. This research provides evidence for an underlying epigenetic mechanism, as the stress response in offspring was determined by the foster mother, not the biological, genetic mother.[22]

Pharmacological research has also demonstrated the reversibility of epigenetic changes related to maternal care in mice. When adult offspring of low licking-grooming mothers were injected with an agent that decreased DNA methylation to match levels of adult pups of high licking-grooming mothers, their responsivity to stress decreased to match the levels seen in the offspring of high licking-grooming mothers.[27] Conversely, when adult offspring of high licking-grooming mothers were injected with an agent to increase DNA methylation, their response to stress increased to match adult offspring of low licking-grooming parents.[28]

Stable epigenetic variations in parental care can be passed down from one generation to the next, from mother to female offspring. Female offspring who received increased parental care (i.e., high licking-grooming) became mothers who engaged in high licking-grooming. Conversely, offspring who received less licking-grooming became mothers who engaged in less licking-grooming. Research has also provided a transgenerational epigenetic link related to maternal care. To this end, offspring of mothers with high licking-grooming behaviour evidenced DNA methylation-related increased expression of an estrogen receptor gene in the medial preoptic region of the hypothalamus – an area of the brain known to be linked to maternal nurturing and care.[29]

In humans, a small clinical research study showed the relationship between prenatal exposure to maternal mood and genetic expression resulting in increased reactivity to stress in offspring. Three groups of infants were examined: those born to mothers medicated for depression with serotonin reuptake inhibitors; those born to depressed mothers not being treated for depression; and those born to non-depressed mothers. Prenatal exposure to depressed/anxious mood was associated with increased epigenetic changes in terms of increased DNA methylation at the glucorticoid receptor gene. In turn, this was related to increased HPA axis stress reactivity - as measured by increased salivary cortisol in three month old infants.[30] Increased cortisol levels are associated with increased stress.[25] The findings were independent of whether the mothers were being pharmaceutically treated for depression.[30]

Cognition

Learning and memory

Studies in rodents have found that the environment exerts an influence on epigenetic changes related to cognition, in terms of learning and memory.[31][32] Animal studies using mice with extensive neurodegeneration and synaptic loss in the forebrain indicated that environmental enrichment helped to restore spatial learning and long-term memories. Specifically, mice with brain damage were subjected to a fear paradigm that consisted of a single exposure to a conditioning context followed by an electric foot shock that elicited a freezing (i.e., staying still) response. After training, the mice rested for four weeks in order to develop long-term memories. Mice were then housed in regular animal cages or in enriched environments for ten weeks. The enriched environments consisted of cages with running wheels, play tunnels, and climbing apparatuses. When re-exposed to the conditioned context, mice housed in regular cages displayed impaired freezing responses. Conversely, the environmentally-enriched mice displayed the freezing behaviour, indicating a recovery of long-term memories.[32]

Other memory-related research has yielded similar results. For example, when placed in a tub of water, brain-damaged mice learned to swim to a platform to escape from the water in the Morris water navigation task. After training, the brain-damaged mice that had resided in regular cages could no longer swim directly to the platform. However, brain-damaged mice that had resided in enriched environments remembered where the platform was located and swam to it – indicating a recovery of long-term memories. The environmental enrichment induced epigenetic changes in the hippocampus and cortex regions (via histone acetylation) of the brain. Injection of histone deacetylase inhibitor was shown to increase hippocampal acetylation and mimic the effects of environmental enrichment in brain-damaged mice by reinstating learning and long-term memory loss. The latter was assessed by the freezing-fear response and performance on the Morris water maze. These findings are consistent with human studies that have noted cognitive fluctuations like temporary periods of clear memories in individuals with dementia.[32] Research has also linked learning and long-term memory formation to reversible epigenetic changes in the hippocampus and cortex in animals with normal-functioning, non-damaged brains.[31][33] In human studies, post-mortem brains from Alzheimer's patients show increased histone de-acetylase levels.[34]

Animal studies have also provided evidence for epigenetic, age-associated memory decline.[31] Older mice show increased epigenetic changes (i.e., decreased histone acetylation and reduced gene expression) in the hippocampus that is related to poorer learning and memory in the Morris water maze. Specifically, older mice require more time to find the platform and escape from the water. Agents used to increase histone acetylation (i.e., reverse the age-related epigenetic effects) improves performance in the older rats.[35]

One review also noted the role of DNA methylation in memory formation and storage, but the precise mechanisms involving neuronal function, memory, and methylation reversal remain unclear.[36]

Psychopathology and mental health

Substance use and addiction

Environmental and epigenetic influences seem to work together to increase the risk of addiction.[37] For example, environmental stress has been shown to increase the risk of substance use.[38] In an attempt to cope with stress, alcohol and drugs can be used as an escape.[39] Once substance use commences, however, epigenetic alterations may further exacerbate the biological and behavioural changes associated with addiction.[37]

Even short-term substance use can produce long-lasting epigenetic changes in the brain of rodents,[37] via DNA methylation and histone modification.[11] Epigenetic modifications have been observed in studies in rodents of alcohol, nicotine, cocaine, amphetamines, and opiate use. Specifically, these epigenetic changes modify gene expression, which in turn increases the vulnerability of an individual to engage in future, repeated substance use. In turn, increased substance use results in even greater epigenetic changes in the rodent brain's pleasure-reward areas[37] (e.g., in the nucleus accumbens[40]). Hence, a cycle emerges whereby changes in the pleasure-reward areas contribute to the long-lasting neural and behavioural changes associated with the increased likelihood of addiction, the maintenance of addiction and relapse.[37] In humans, alcohol consumption has been shown to produce epigenetic changes that contribute to the increased craving of alcohol. As such, epigenetic modifications may play a part in the progression from the controlled intake to the loss of control of alcohol consumption.[41] These alterations may be long-term, as is evidenced in smokers who still possess nicotine-related epigenetic changes ten years after cessation.[42] Therefore, epigenetic modifications[37] may account for some of the behavioural changes generally associated with addiction. These include: repetitive habits that increase the risk of disease, and personal and social problems; need for immediate gratification; high rates of relapse following treatment; and, the feeling of loss of control.[43]

Evidence for related epigenetic changes has come from human studies on alcohol,[44] nicotine and opiate use. Evidence for epigenetic changes stemming from amphetamine and cocaine use derives from animal studies. In animals, drug-related epigenetic changes in fathers have also been shown to negatively affect offspring in terms of poorer spatial working memory, decreased attention and decreased cerebral volume.[45]

Eating disorders and obesity

Epigenetic changes may help to facilitate the development and maintenance of eating disorders via influences in the early environment and throughout the life-span.[15] Pre-natal epigenetic changes due to maternal stress, behaviour and diet may later predispose offspring to persistent, increased anxiety and anxiety disorders. These anxiety issues can precipitate the onset of eating disorders and obesity, and persist even after recovery from the eating disorders.[46]

Epigenetic differences accumulating over the life-span may account for the incongruent differences in eating disorders observed in monozygotic twins. At puberty, sex hormones may exert epigenetic changes (via DNA methylation) on gene expression, thus accounting for higher rates of eating disorders in men as compared to women. Overall, epigenetics contribute to persistent, unregulated self-control behaviours related to the urge to binge.[15]

Schizophrenia

For more details on this topic, see Epigenetics of schizophrenia.

Epigenetic changes including hypomethylation of glutamatergic genes (i.e., NMDA-receptor-subunit gene NR3B and the promoter of the AMPA-receptor-subunit gene GRIA2) in the post-mortem human brains of schizophrenics are associated with increased levels of the neurotoxin glutamate.[47] Since glutamate is the most prevalent, fast, excitatory neurotoxin, increased levels may result in the psychotic episodes related to schizophrenia. Interestingly, epigenetic changes affecting a greater number of genes have been detected in men with schizophrenia as compared to women with the illness.[48]

Population studies have established a strong association linking schizophrenia in children born to older fathers.[49][50] Specifically, children born to fathers over the age of 35 years are up to three times more likely to develop schizophrenia.[50] Epigenetic dysfunction in human male sperm cells, affecting numerous genes, have been shown to increase with age. This provides a possible explanation for increased rates of the disease in men.[48][50][failed verification] To this end, toxins[48][50] (e.g., air pollutants) have been shown to increase epigenetic differentiation. Animals exposed to ambient air from steel mills and highways show drastic epigenetic changes that persist after removal from the exposure.[51] Therefore, similar epigenetic changes in older human fathers are likely.[50] Schizophrenia studies provide evidence that the nature versus nurture debate in the field of psychopathology should be re-evaluated to accommodate the concept that genes and the environment work in tandem. As such, many other environmental factors (e.g., nutritional deficiencies and cannabis use) have been proposed to increase the susceptibility of psychotic disorders like schizophrenia via epigenetics.[50]

Bipolar disorder

Evidence for epigenetic modifications for bipolar disorder is unclear.[52] One study found hypomethylation of a gene promoter of a prefrontal lobe enzyme (i.e., membrane-bound catechol-O-methyl transferase, or COMT) in post-mortem brain samples from individuals with bipolar disorder. COMT is an enzyme that metabolizes dopamine in the synapse. These findings suggest that the hypomethylation of the promoter results in over-expression of the enzyme. In turn, this results in increased degradation of dopamine levels in the brain. These findings provide evidence that epigenetic modification in the prefrontal lobe is a risk factor for bipolar disorder.[53] However, a second study found no epigenetic differences in post-mortem brains from bipolar individuals.[54]

Major Depressive Disorder

The full pathology of Major Depressive Disorder (MDD) has yet to be fully elucidated[55], however research on Brain Derived Neurotrophic Factor (bdnf) has provided evidence of its relation to MDD and its control, in part, by epigenetic modification.[56] bdnf is a protein that is part of the neurotrophin class of growth factors that acts to induce neuron regeneration and neuroplasticity for nerves in both the central and peripheral nervous system.[57] It does this by binding to thetrkB receptor, which is a protein receptor found in the cell membrane of cells located in the central and peripheral nervous system, however trkB is most predominantly found in the brain.[58] Once bdnf is bound to trkB, a cascade of downstream effectors act to increase cell regeneration and neural plasticity.

bdnf acts as a neuroprotective factor on sections of the HPA axis whose degeneration may cause depression.[59][60] While human studies have demonstrated decreased levels of bdnf in patients who have MDD or have committed suicide[61][62], murine studies have painted a clearer picture of the epigenetic mechanisms relating bdnf to MDD. The main exogenic contributing factor to epigenetic remodelling of bdnf in the HPA axis is chronic stress[63], which is a known mediating factor of depression.[64] Corticosteroid hormone release as a result of stress acts to methylate at a repressive histone mark on histone 3 at promoter regions of the BDNF gene.[65] Therefore, as a subject is exposed to chronic stress, glucocorticoids may act to cause both acute neural atrophy as well as induce long-term histone methylation and therefore under-expression, leading to depression.[66]

Psychopathy

Epigenetics may be relevant to aspects of psychopathic behaviour through methylation and histone modification.[67] These processes are heritable but can also be influenced by environmental factors such as smoking and abuse.[68] Epigenetics may be one of the mechanisms through which the environment can impact the expression of the genome.[69] Studies have also linked methylation of genes associated with nicotine and alcohol dependence in women, ADHD, and drug abuse.[70] [71] [72] It is probable that epigenetic regulation as well as methylation profiling will play an increasingly important role in the study of the play between the environment and genetics of psychopaths.[73]

Suicide

People who commit suicide have less-active ribosomal RNA (rRNA) genes than people who die of other causes. Methyl levels of suicide victims are higher on rRNA genes in the Hippocamous of the brain, associated with learning and memory.[74] More methyl means less rRNA production,limiting the number of ribosomes and decreasing protein production.[75]

Early life experiences such as Familial function and childhood adversity are linked to altered HPA stress responses in humans.[76] Child abuse is an environmental factor that leaves an epigenetic mark on the brain. In a comparison of suicide victims who were abused or not, only the abused victims had an epigenetic tag on the GR gene.[77]There is evidence for decreased hippocampal glucocorticoid receptor expression in several psychopathological conditions associated with suicide, including schizophrenia and mood disorders. Suicide is also strongly associated with a history of childhood abuse and neglect. Thus, environmental events that associate with decreased hippocampal glucocorticoid receptor expression and increased HPA activity enhance the risk of suicide.[78]

Limitations and future direction

Many researchers contribute information to the Human Epigenome Consortium.[79] The aim of future research is to reprogram epigenetic changes to help with addiction, mental illness, age related changes,[1] memory decline, and other issues.[31] However, the sheer volume of consortium-based data makes analysis difficult.[1] Most studies also focus on one gene.[26] In actuality, many genes and interactions between them likely contribute to individual differences in personality, behaviour and health.[80] As social scientists often work with many variables, determining the number of affected genes also poses methodological challenges. More collaboration between medical researchers, geneticists and social scientists has been advocated to increase knowledge in this field of study.[81]

Limited access to human brain tissue poses a challenge to conducting human research.[1] Not yet knowing if epigenetic changes in the blood and (non-brain) tissues parallel modifications in the brain, places even greater reliance on brain research.[79] Although some epigenetic studies have translated findings from animals to humans,[82] some researchers caution about the extrapolation of animal studies to humans.[31] One view notes that when animal studies do not consider how the subcellular and cellular components, organs and the entire individual interact with the influences of the environment, results are too reductive to explain behaviour.[80]

Some researchers note that epigenetic perspectives will likely be incorporated into pharmacological treatments.[6] Others caution that more research is necessary as drugs are known to modify the activity of multiple genes and may, therefore, cause serious side effects.[31] However, the ultimate goal is to find patterns of epigenetic changes that can be targeted to treat mental illness, and reverse the effects of childhood stressors, for example. If such treatable patterns eventually become well-established, the inability to access brains in living humans to identify them poses an obstacle to pharmacological treatment.[79] Future research may also focus on epigenetic changes that mediate the impact of psychotherapy on personality and behaviour.[22]

Most epigenetic research is cross-sectional in that it establishes associations. More longitudinal research is necessary to help establish causation.[83] Lack of resources has also limited the number of intergenerational studies.[1] Therefore, advancing longitudinal[81] and multigenerational, experience-dependent studies will be critical to further understanding the role of epigenetics in psychology.[3]

See also

References

  1. ^ a b c d e f g Powledge T (2011). "Behavioral epigenetics: How nurture shapes nature". BioScience. 61 (8): 588–592. doi:10.1525/bio.2011.61.8.4.
  2. ^ Kail RV, Barnfield A (2011). Children and Their Development, Second Canadian Edition with MyDevelopmentLab. Toronto: Pearson Education Canada. ISBN 0-13-255770-3.
  3. ^ a b Champagne FA, Mashoodh R (2012). "Genes in context: Gene-environment interplay and the origins of individual differences in behaviour" (PDF). Current Directions in Psychological Science. 18 (3): 127–131. doi:10.1111/j.1467-8721.2009.01622.x.
  4. ^ Zhang TY, Meaney MJ (2010). "Epigenetics and the environmental regulation of the genome and its function". Annu Rev Psychol. 61: 439–66, C1–3. doi:10.1146/annurev.psych.60.110707.163625. PMID 19958180.
  5. ^ Cite error: The named reference Bagot_2010 was invoked but never defined (see the help page).
  6. ^ a b Stuffrein-Roberts S, Joyce PR, Kennedy MA (2008). "Role of epigenetics in mental disorders". Aust N Z J Psychiatry. 42 (2): 97–107. doi:10.1080/00048670701787495. PMID 18197504. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  7. ^ Mill J, Tang T, Kaminsky Z, Khare T, Yazdanpanah S, Bouchard L, Jia P, Assadzadeh A, Flanagan J, Schumacher A, Wang SC, Petronis A (2008). "Epigenomic profiling reveals DNA-methylation changes associated with major psychosis". Am. J. Hum. Genet. 82 (3): 696–711. doi:10.1016/j.ajhg.2008.01.008. PMC 2427301. PMID 18319075. {{cite journal}}: Unknown parameter |laysource= ignored (help); Unknown parameter |laysummary= ignored (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Bird A (2007). "Perceptions of epigenetics". Nature. 447 (7143): 396–8. Bibcode:2007Natur.447..396B. doi:10.1038/nature05913. PMID 17522671. {{cite journal}}: Unknown parameter |month= ignored (help)
  9. ^ NIH Roadmap Epigenomics Project Overview
  10. ^ Mehler MF (2008). "Epigenetic principles and mechanisms underlying nervous system functions in health and disease". Prog. Neurobiol. 86 (4): 305–41. doi:10.1016/j.pneurobio.2008.10.00. PMC 2636693. PMID 18940229. {{cite journal}}: Unknown parameter |month= ignored (help)
  11. ^ a b Maze I, Nestler EJ (2011). "The epigenetic landscape of addiction". Ann. N. Y. Acad. Sci. 1216: 99–113. doi:10.1111/j.1749-6632.2010.05893.x. PMC 3071632. PMID 21272014. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ Reik W (2007). "Stability and flexibility of epigenetic gene regulation in mammalian development". Nature. 447 (7143): 425–32. doi:10.1038/nature05918. PMID 17522676. {{cite journal}}: Unknown parameter |month= ignored (help)
  13. ^ Gottesman II, Hanson DR (2005). "Human development: biological and genetic processes". Annu Rev Psychol. 56: 263–86. doi:10.1146/annurev.psych.56.091103.070208. PMID 15709936.
  14. ^ Cite error: The named reference pmid11498570 was invoked but never defined (see the help page).
  15. ^ a b c Cite error: The named reference Campbell_2011 was invoked but never defined (see the help page).
  16. ^ a b Goto T, Monk M (1998). "Regulation of X-chromosome inactivation in development in mice and humans". Microbiol. Mol. Biol. Rev. 62 (2): 362–78. PMC 98919. PMID 9618446. {{cite journal}}: Unknown parameter |month= ignored (help)
  17. ^ a b c d e f g Kaminsky Z, Petronis A, Wang SC, Levine B, Ghaffar O, Floden D, Feinstein A (2008). "Epigenetics of personality traits: an illustrative study of identical twins discordant for risk-taking behavior". Twin Res Hum Genet. 11 (1): 1–11. doi:10.1375/twin.11.1.1. PMID 18251670. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  18. ^ Kovács KJ, Miklós IH, Bali B (2004). "GABAergic mechanisms constraining the activity of the hypothalamo-pituitary-adrenocortical axis". Ann. N. Y. Acad. Sci. 1018: 466–76. doi:10.1196/annals.1296.057. PMID 15240403. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  19. ^ Cobos I, Broccoli V, Rubenstein JL (2005). "The vertebrate ortholog of Aristaless is regulated by Dlx genes in the developing forebrain". J. Comp. Neurol. 483 (3): 292–303. doi:10.1002/cne.20405. PMID 15682394. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  20. ^ Kash TL, Winder DG (2006). "Neuropeptide Y and corticotropin-releasing factor bi-directionally modulate inhibitory synaptic transmission in the bed nucleus of the stria terminalis". Neuropharmacology. 51 (5): 1013–22. doi:10.1016/j.neuropharm.2006.06.011. PMID 16904135. {{cite journal}}: Unknown parameter |month= ignored (help)
  21. ^ Gutman DA, Nemeroff DB (2010). "Stress and depression". In Baum A, Contrada RJ (ed.). The Handbook of Stress Science: Biology, Psychology, and Health. New York: Springer Publishing Company. p. 347. ISBN 0-8261-1471-7.
  22. ^ a b c d e f Masterpasqua F (2009). "Psychology and epigenetics". Reveiw of General Psychology. 13 (3): 194–201. doi:10.1037/a0016301.
  23. ^ a b c Szyf M, McGowan P, Meaney MJ (2008). "The social environment and the epigenome" (PDF). Environ. Mol. Mutagen. 49 (1): 46–60. doi:10.1002/em.20357. PMID 18095330. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  24. ^ Cite error: The named reference Guyton was invoked but never defined (see the help page).
  25. ^ a b Parkinson CF, McCance KL, Huether SE (1997). Pathophysiology : The Biologic Basis for Disease in Adults and Children (Study Guide & Workbook). St. Louis, USA: Mosby Elsevier Health Science. ISBN 0-8151-3766-4.{{cite book}}: CS1 maint: multiple names: authors list (link)
  26. ^ a b Baum A, Contrada RJ (2010). The Handbook of Stress Science: Biology, Psychology, and Health. New York: Springer Publishing Company. pp. 77–100. ISBN 0-8261-1471-7. Cite error: The named reference "McCaffery" was defined multiple times with different content (see the help page).
  27. ^ Weaver IC, Cervoni N, Champagne FA, D'Alessio AC, Sharma S, Seckl JR, Dymov S, Szyf M, Meaney MJ (2004). "Epigenetic programming by maternal behavior". Nat. Neurosci. 7 (8): 847–54. doi:10.1038/nn1276. PMID 15220929. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  28. ^ Weaver IC, Champagne FA, Brown SE, Dymov S, Sharma S, Meaney MJ, Szyf M (2005). "Reversal of maternal programming of stress responses in adult offspring through methyl supplementation: altering epigenetic marking later in life". J. Neurosci. 25 (47): 11045–54. doi:10.1523/JNEUROSCI.3652-05.2005. PMID 16306417. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  29. ^ Champagne FA, Weaver IC, Diorio J, Dymov S, Szyf M, Meaney MJ (2006). "Maternal care associated with methylation of the estrogen receptor-alpha1b promoter and estrogen receptor-alpha expression in the medial preoptic area of female offspring". Endocrinology. 147 (6): 2909–15. doi:10.1210/en.2005-1119. PMID 16513834. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  30. ^ a b Oberlander TF, Weinberg J, Papsdorf M, Grunau R, Misri S, Devlin AM (2008). "Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses". Epigenetics. 3 (2): 97–106. PMID 18536531.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ a b c d e f Miller G (2010). "Epigenetics. The seductive allure of behavioral epigenetics". Science. 329 (5987): 24–7. doi:10.1126/science.329.5987.24. PMID 20595592. {{cite journal}}: Unknown parameter |month= ignored (help)
  32. ^ a b c Fischer A, Sananbenesi F, Wang X, Dobbin M, Tsai LH (2007). "Recovery of learning and memory is associated with chromatin remodelling". Nature. 447 (7141): 178–82. doi:10.1038/nature05772. PMID 17468743. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  33. ^ Gupta S, Kim SY, Artis S, Molfese DL, Schumacher A, Sweatt JD, Paylor RE, Lubin FD (2010). "Histone methylation regulates memory formation". J. Neurosci. 30 (10): 3589–99. doi:10.1523/JNEUROSCI.3732-09.2010. PMC 2859898. PMID 20219993. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  34. ^ Gräff J, Rei D, Guan JS, Wang WY, Seo J, Hennig KM, Nieland TJ, Fass DM, Kao PF, Kahn M, Su SC, Samiei A, Joseph N, Haggarty SJ, Delalle I, Tsai LH (2012). "An epigenetic blockade of cognitive functions in the neurodegenerating brain". Nature. 483 (7388): 222–6. doi:10.1038/nature10849. PMID 22388814. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  35. ^ Peleg S, Sananbenesi F, Zovoilis A, Burkhardt S, Bahari-Javan S, Agis-Balboa RC, Cota P, Wittnam JL, Gogol-Doering A, Opitz L, Salinas-Riester G, Dettenhofer M, Kang H, Farinelli L, Chen W, Fischer A (2010). "Altered histone acetylation is associated with age-dependent memory impairment in mice". Science. 328 (5979): 753–6. doi:10.1126/science.1186088. PMID 20448184. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  36. ^ Day JJ, Sweatt JD (2010). "DNA methylation and memory formation". Nat. Neurosci. 13 (11): 1319–23. doi:10.1038/nn.2666. PMC 3130618. PMID 20975755. {{cite journal}}: Unknown parameter |month= ignored (help)
  37. ^ a b c d e f Wong CC, Mill J, Fernandes C (2011). "Drugs and addiction: an introduction to epigenetics". Addiction. 106 (3): 480–9. doi:10.1111/j.1360-0443.2010.03321.x. PMID 21205049. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  38. ^ Andersen SL, Teicher MH (2009). "Desperately driven and no brakes: developmental stress exposure and subsequent risk for substance abuse". Neurosci Biobehav Rev. 33 (4): 516–24. doi:10.1016/j.neubiorev.2008.09.009. PMC 2688959. PMID 18938197. {{cite journal}}: Unknown parameter |month= ignored (help)
  39. ^ Carver C (2010). "Coping". In Baum A, Contrada RJ (ed.). The Handbook of Stress Science: Biology, Psychology, and Health. New York: Springer Publishing Company. p. 223. ISBN 0-8261-1471-7.
  40. ^ Renthal W, Nestler EJ (2008). "Epigenetic mechanisms in drug addiction". Trends Mol Med. 14 (8): 341–50. doi:10.1016/j.molmed.2008.06.004. PMC 2753378. PMID 18635399. {{cite journal}}: Unknown parameter |month= ignored (help)
  41. ^ Naassila M (2011). "Epigenetics in alcohol addiction: New mechanisms for new treatments?". Alcohol and Alcoholism. 46 (Suppl 1): i1–63. doi:10.1093/alcalc/agr085. PMID 21863600.
  42. ^ Launay JM, Del Pino M, Chironi G, Callebert J, Peoc'h K, Mégnien JL, Mallet J, Simon A, Rendu F (2009). "Smoking induces long-lasting effects through a monoamine-oxidase epigenetic regulation". PLoS ONE. 4 (11): e7959. doi:10.1371/journal.pone.0007959. PMC 2775922. PMID 19956754.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  43. ^ Marlatt GA, Baer JS, Donovan DM, Kivlahan DR (1988). "Addictive behaviors: etiology and treatment". Annu Rev Psychol. 39: 223–52. doi:10.1146/annurev.ps.39.020188.001255. PMID 3278676.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  44. ^ Bönsch D, Lenz B, Reulbach U, Kornhuber J, Bleich S (2004). "Homocysteine associated genomic DNA hypermethylation in patients with chronic alcoholism". J Neural Transm. 111 (12): 1611–6. doi:10.1007/s00702-004-0232-x. PMID 15565495. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  45. ^ He F, Lidow IA, Lidow MS (2006). "Consequences of paternal cocaine exposure in mice". Neurotoxicol Teratol. 28 (2): 198–209. doi:10.1016/j.ntt.2005.12.003. PMID 16458479.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  46. ^ Raney TJ, Thornton LM, Berrettini W, Brandt H, Crawford S, Fichter MM, Halmi KA, Johnson C, Kaplan AS, LaVia M, Mitchell J, Rotondo A, Strober M, Woodside DB, Kaye WH, Bulik CM (2008). "Influence of overanxious disorder of childhood on the expression of anorexia nervosa". Int J Eat Disord. 41 (4): 326–32. doi:10.1002/eat.20508. PMID 18213688. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  47. ^ Cite error: The named reference Mostafavi-Abdolmaleky was invoked but never defined (see the help page).
  48. ^ a b c Abdolmaleky HM, Thiagalingam S, Wilcox M (2005). "Genetics and epigenetics in major psychiatric disorders: dilemmas, achievements, applications, and future scope". Am J Pharmacogenomics. 5 (3): 149–60. PMID 15952869.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Malaspina D, Harlap S, Fennig S, Heiman D, Nahon D, Feldman D, Susser ES (2001). "Advancing paternal age and the risk of schizophrenia". Arch. Gen. Psychiatry. 58 (4): 361–7. doi:10.1001/archpsyc.58.4.361. PMID 11296097. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  50. ^ a b c d e f Rutten BP, Mill J (2009). "Epigenetic mediation of environmental influences in major psychotic disorders". Schizophr Bull. 35 (6): 1045–56. doi:10.1093/schbul/sbp104. PMC 2762629. PMID 19783603. {{cite journal}}: Unknown parameter |month= ignored (help)
  51. ^ Yauk C, Polyzos A, Rowan-Carroll A, Somers CM, Godschalk RW, Van Schooten FJ, Berndt ML, Pogribny IP, Koturbash I, Williams A, Douglas GR, Kovalchuk O (2008). "Germ-line mutations, DNA damage, and global hypermethylation in mice exposed to particulate air pollution in an urban/industrial location". Proc. Natl. Acad. Sci. U.S.A. 105 (2): 605–10. doi:10.1073/pnas.0705896105. PMC 2206583. PMID 18195365. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  52. ^ McGowan PO, Kato T (2008). "Epigenetics in mood disorders". Environ Health Prev Med. 13 (1): 16–24. doi:10.1007/s12199-007-0002-0. PMC 2698240. PMID 19568875. {{cite journal}}: Unknown parameter |month= ignored (help)
  53. ^ Abdolmaleky HM, Cheng KH, Faraone SV, Wilcox M, Glatt SJ, Gao F, Smith CL, Shafa R, Aeali B, Carnevale J, Pan H, Papageorgis P, Ponte JF, Sivaraman V, Tsuang MT, Thiagalingam S (2006). "Hypomethylation of MB-COMT promoter is a major risk factor for schizophrenia and bipolar disorder". Hum. Mol. Genet. 15 (21): 3132–45. doi:10.1093/hmg/ddl253. PMC 2799943. PMID 16984965. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  54. ^ Dempster EL, Mill J, Craig IW, Collier DA (2006). "The quantification of COMT mRNA in post mortem cerebellum tissue: diagnosis, genotype, methylation and expression". BMC Med. Genet. 7: 10. doi:10.1186/1471-2350-7-10. PMC 1456954. PMID 16483362.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  55. ^ Wainwright SR, Galea LAM (2013). "The Neural Plasticity Theory of Depression: Assessing the Roles of Adult Neurogenesis and PSA-NCAM within the Hippocampus". Neural Plasticity. 2013: 1–14. doi:10.1155/2013/805497.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  56. ^ Villanueva R (2013). "Neurobiology of Major Depressive Disorder". Neural Plasticity. 2013: 1–7. doi:10.1155/2013/873278.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  57. ^ Huang EJ, Reichardt LF (2001). "Neurotrophins: Roles in Neuronal Development and Function" (PDF). Annu Rev Neurosci. 24: 677–736. doi:10.1146/annurev.neuro.24.1.677. {{cite journal}}: Check |doi= value (help)
  58. ^ http://www.uniprot.org/uniprot/Q16620
  59. ^ Pariante CM, Lightman CL (2008). "The HPA axis in major depression: classical theories and new developments". Trends In Neurosciences. 31 (9): 464–468. doi:10.1016/j.tins.2008.06.006.
  60. ^ Massart R, Mongeau R, Lanfumey L (2012). "Beyond the monoaminergic hypothesis:neuroplasticity and epigenetic changes in a transgenic mouse model of depression" (PDF). Phil. Trans. R. Soc. B. 367: 2485–2494. doi:10.1098/rstb.2012.0212.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  61. ^ Karege F, Perret G, Bondolfi G, Schwald M, Bertschy G, Aubry JM (2002). "Decreased serum brain-derived neurotrophic factor levels in major depressed patients". Psychiatry Research. 109: 143–148. doi:10.1016/S0165-1781(02)00005-7.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  62. ^ Dwivedi Y, Rizavi HS, Conley RR, Roberts RC, Tamminga CA, Pandey GN (2003). "Altered Gene Expression of Brain-Derived Neurotrophic Factor and Receptor Tyrosine Kinase B in Postmortem Brain of Suicide Subjects". Arch Gen Psychiatry. 60 (8): 804–815. doi:10.1001/archpsyc.60.8.804.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  63. ^ Tsankova NM, Berton O, Renthal W, Kumar A, Neve RL, Nestler EJ. (2006). "Sustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action". Nat. Neurosci. 9 (4): 519–525. doi:10.1038/nn1659.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  64. ^ Tapia-Arancibia L, Rage F, Givalois L, Arancibia S (2004). "Physiology of BDNF: focus on hypothalamic function". Frontiers in Neuroendocrinology. 25: 77–107. doi:10.1016/j.yfrne.2004.04.001.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  65. ^ Hunter RG (2012). "Epigenetic effects of stress and corticosteroids in the brain". Front. Cell. Neurosci. 6: 1–8. doi:10.3389/fncel.2012.00018.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  66. ^ Gray JD, Milner TA, McEwen BS (2013). "DYNAMIC PLASTICITY: THE ROLE OF GLUCOCORTICOIDS,BRAIN-DERIVED NEUROTROPHIC FACTOR AND OTHER TROPHIC FACTORS". Neuroscience. 239: 214–227. doi:10.1016/j.neuroscience.2012.08.034.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  67. ^ Jiang, Y. (12 November 2008). "Epigenetics in the Nervous System". Journal of Neuroscience. 28 (46): 11753–11759. doi:10.1523/JNEUROSCI.3797-08.2008. PMID 19005036. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  68. ^ Philibert, Robert A. (1 January 2009). "The effect of smoking on promoter methylation in DNA prepared from lymphoblasts and whole blood". American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 9999B: n/a–n/a. doi:10.1002/ajmg.b.31031. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  69. ^ Philibert, Robert A. (5 July 2008). "The relationship of ( ) methylation and genotype on mRNA expression and liability to major depression and alcohol dependence in subjects from the Iowa Adoption Studies". American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 147B (5): 543–549. doi:10.1002/ajmg.b.30657. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  70. ^ Philibert, Robert A. (5 July 2008). "MAOA methylation is associated with nicotine and alcohol dependence in women". American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 147B (5): 565–570. doi:10.1002/ajmg.b.30778. PMID 18454435. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  71. ^ Bodnar, Richard J. (1 December 2010). "Endogenous opiates and behavior: 2009". Peptides. 31 (12): 2325–2359. doi:10.1016/j.peptides.2010.09.016.
  72. ^ Mill, Jonathan (1 October 2008). "Pre- and peri-natal environmental risks for attention-deficit hyperactivity disorder (ADHD): the potential role of epigenetic processes in mediating susceptibility". Journal of Child Psychology and Psychiatry. 49 (10): 1020–1030. doi:10.1111/j.1469-7610.2008.01909.x. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  73. ^ Gunter, Tracy D. (1 March 2010). "Behavioral genetics in antisocial spectrum disorders and psychopathy: A review of the recent literature". Behavioral Sciences & the Law. 28 (2): 148–173. doi:10.1002/bsl.923. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  74. ^ Epigenetics and the Human Brain. (n.d.). Learn.Geneticsâ„¢. Retrieved September 25, 2013, from http://learn.genetics.utah.edu/content/epigenetics/brain/
  75. ^ Epigenetics and the Human Brain. (n.d.). Learn.Geneticsâ„¢. Retrieved September 25, 2013, from http://learn.genetics.utah.edu/content/epigenetics/brain/
  76. ^ McGowan, P., Sasaki, A., & Meaney, M. (2009). Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nature Neuroscience, 12(3), 342-348. Retrieved September 25, 2013, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2944040/#__ffn_sectitle
  77. ^ Epigenetics and the Human Brain. (n.d.). Learn.Geneticsâ„¢. Retrieved September 25, 2013, from http://learn.genetics.utah.edu/content/epigenetics/brain/
  78. ^ McGowan, P., Sasaki, A., & Meaney, M. (2009). Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nature Neuroscience, 12(3), 342-348. Retrieved September 25, 2013, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2944040/#__ffn_sectitle
  79. ^ a b c Albert PR (2010). "Epigenetics in mental illness: hope or hype?". J Psychiatry Neurosci. 35 (6): 366–8. doi:10.1503/jpn.100148. PMC 2964366. PMID 20964959. {{cite journal}}: Unknown parameter |month= ignored (help)
  80. ^ a b Kalant H (2010). "What neurobiology cannot tell us about addiction". Addiction. 105 (5): 780–9. doi:10.1111/j.1360-0443.2009.02739.x. PMID 19919596. {{cite journal}}: Unknown parameter |month= ignored (help)
  81. ^ a b Guo G (2010). "Family influences on children's well being: potential roles of molecular genetics and epigenetics". In Landale N, Booth A, McHale S (ed.). Biosocial Foundations of Family Processes (National Symposium on Family Issues). Berlin: Springer. pp. 181–204. ISBN 1-4419-7360-5.{{cite book}}: CS1 maint: multiple names: editors list (link)
  82. ^ McGowan PO, Sasaki A, D'Alessio AC, Dymov S, Labonté B, Szyf M, Turecki G, Meaney MJ (2009). "Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse". Nat. Neurosci. 12 (3): 342–8. doi:10.1038/nn.2270. PMC 2944040. PMID 19234457. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  83. ^ Dempster EL, Pidsley R, Schalkwyk LC, Owens S, Georgiades A, Kane F, Kalidindi S, Picchioni M, Kravariti E, Toulopoulou T, Murray RM, Mill J (2011). "Disease-associated epigenetic changes in monozygotic twins discordant for schizophrenia and bipolar disorder". Hum. Mol. Genet. 20 (24): 4786–96. doi:10.1093/hmg/ddr416. PMC 3221539. PMID 21908516. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

Further reading

  • McDonald B (2011). "The Fingerprints of Poverty". Quirks & Quarks. CBC Radio. Audio interview with Moshe Szyf, a professor of Pharmacology and Therapeutics at McGill University, discusses how epigenetic changes are related to differences in socioeconomic status.
  • Oz M (2011). "Control Your Pregnancy". The Dr. Oz Show. Video explaining how epigenetics can affect the unborn fetus.
  • Paylor B (2010). "Epigenetic Landscapes". This video addresses how, in principle, accumulated epigenetic changes may result in personality differences in identical twins. This video was made by a Ph.D. candidate in experimental medicine and award winning filmmaker Ben Paylor.
  • Rusting R (2011). "Epigenetics Explained (Animation)". Scientific American Magazine. A series of diagrams explaining how epigenetic marks affect genetic expression. {{cite web}}: Italic or bold markup not allowed in: |publisher= (help)
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