DNA methylation, the early-life social environment and behavioral disorders

被引:43
作者
Szyf, Moshe [1 ,2 ]
机构
[1] McGill Univ, Sackler Program Epigenet & Psychobiol, Montreal, PQ H3G 1Y6, Canada
[2] McGill Univ, Dept Pharmacol & Therapeut, Montreal, PQ H3G 1Y6, Canada
基金
加拿大健康研究院;
关键词
DNA methylation; Epigenetics; Development; Demethylation; Behavioral disorders; Epigenome; INHIBITS ACTIVE DEMETHYLATION; TRANSCRIPTIONAL REPRESSOR; GLUCOCORTICOID-RECEPTOR; BDNF TRANSCRIPTION; STRESS RESPONSES; FRONTAL-CORTEX; MATERNAL-CARE; COPY-NUMBER; GERM-CELLS; GENE;
D O I
10.1007/s11689-011-9079-2
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
One of the outstanding questions in behavioral disorders is untangling the complex relationship between nurture and nature. Although epidemiological data provide evidence that there is an interaction between genetics (nature) and the social and physical environments (nurture) in a spectrum of behavioral disorders, the main open question remains the mechanism. Emerging data support the hypothesis that DNA methylation, a covalent modification of the DNA molecule that is a component of its chemical structure, serves as an interface between the dynamic environment and the fixed genome. We propose that modulation of DNA methylation in response to environmental cues early in life serves as a mechanism of life-long genome adaptation. Under certain contexts, this adaptation can turn maladaptive resulting in behavioral disorders. This hypothesis has important implications on understanding, predicting, preventing, and treating behavioral disorders including autism that will be discussed.
引用
收藏
页码:238 / 249
页数:12
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