DNA METHYLATION AND CHILDHOOD MALTREATMENT: FROM ANIMAL MODELS TO HUMAN STUDIES

被引：96

作者：

Lutz, P-E ^{[1
]}

Turecki, G. ^{[1
]}

机构：

[1] Douglas Mental Hlth Univ Inst, McGill Grp Suicide Studies, Montreal, PQ, Canada

来源：

NEUROSCIENCE | 2014年 / 264卷

基金：

加拿大健康研究院;

关键词：

childhood maltreatment; maternal care; epigenetic; DNA methylation; glucocorticoid receptor; stress; RECEPTOR GENE NR3C1; POSTTRAUMATIC-STRESS-DISORDER; PATERNAL DEPRIVATION ALTERS; ADULT PSYCHIATRIC-DISORDERS; EARLY-LIFE EXPERIENCE; MATERNAL-CARE; GLUCOCORTICOID-RECEPTOR; PHYSICAL ABUSE; EPIGENETIC REGULATION; PREFRONTAL CORTEX;

D O I：

10.1016/j.neuroscience.2013.07.069

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Childhood maltreatment (CM) has estimated prevalence among Western societies between 10% and 15%. As CM associates with increased risk of several psychiatric disorders, early age of illness onset, increased comorbidity and negative clinical outcome, it imposes a major public health, social and economic impact. Although the clinical consequences of CM are well characterized, a major challenge remains to understand how negative early-life events can affect brain function over extended periods of time. We review here both animal and human studies indicating that the epigenetic mechanism of DNA methylation is a crucial mediator of early-life experiences, thereby maintaining life-long neurobiological sequelae of CM, and strongly determining psychopathological risk. This article is part of a Special Issue entitled: Epigenetics in Brain Function. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.

引用

页码：142 / 156

页数：15

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