Early-life stress interactions with the epigenome: potential mechanisms driving vulnerability toward psychiatric illness

Behav Pharmacol. 2014 Sep;25(5-6):341-51. doi: 10.1097/FBP.0000000000000057.

Abstract

Throughout the 20th century a body of literature concerning the long-lasting effects of the early environment was produced. Adverse experiences in early life, or early-life stress (ELS), is associated with a higher risk of developing various psychiatric illnesses. The mechanisms driving the complex interplay between ELS and adult phenotype has baffled many investigators for decades. Over the last decade, the new field of neuroepigenetics has emerged as one possible mechanism by which ELS can have far-reaching effects on adult phenotype, behavior, and risk for psychiatric illness. Here we review two commonly investigated epigenetic mechanisms, histone modifications and DNA methylation, and the emerging field of neuroepigenetics as they relate to ELS. We discuss the current animal literature demonstrating ELS-induced epigenetic modulation of gene expression that results in altered adult phenotypes. We also briefly discuss other areas in which neuroepigenetics has emerged as a potential mechanism underlying environmental and genetic interactions.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain / growth & development
  • Brain / physiopathology
  • DNA Methylation*
  • Histones / metabolism*
  • Humans
  • Mental Disorders / drug therapy
  • Mental Disorders / genetics*
  • Mental Disorders / physiopathology*
  • Risk
  • Stress, Psychological / drug therapy
  • Stress, Psychological / genetics*
  • Stress, Psychological / physiopathology*

Substances

  • Histones