Epigenetics: A Missing Link Between Early Life Stress and Depression

Abstract

Exposure to early life stress (ELS) represents a major risk factor for the development of psychiatric disorders, including depression. The susceptibility associated with ELS may result from persistent changes in gene transcription, which can occur through epigenetic mechanisms, such as DNA methylation, histone modifications, and microRNA expression. Animal models and reports in humans described that negative stimuli can alter the neurodevelopment of an individual, affecting their behavior and cognitive development. It is currently hypothesized that levels of environmental adversity in this early developmental period are able to shape the experience-dependent maturation of stress-regulating pathways leading to long-lasting alterations in stress responsivity during adulthood. Here, we review key findings from animal and clinical studies examining the effects of prenatal and postnatal environment in shaping development of the neuroendocrine regulation of stress and the role of epigenetic mechanisms in the predisposition of depression.