Early Life Stress-Induced Epigenetic Changes Involved in Mental Disorders

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Background

Early life stress has been proposed by many researchers to be a critical causal factor for many types of mental disorders later in life such as depression, anxiety, and post-traumatic stress. However, the underlying neural mechanisms are far from clear. Exposure to stress during critical periods in development can cause severe long-term neural changes, for example changes to the hypothalamic-pituitary-adrenal (HPA) axis, which is a cascade of neural hormone changes resulting in the release of corticosteroids. Corticosteroids affect brain functioning to ensure proper physiological and behavioral responses to stressors, but overwhelming activation of the HPA-axis can induce affective disorders. Early life (i.e., perinatal) exposure to stress has been reported to have numerous effects on the adult HPA-axis, including either beneficial or disadvantageous effects depending on the surrounding environment. Maternal separation, which means temporarily separating offspring from their mothers during lactation, has been an important method of studying early life stress in animals. Fragmented maternal care typically results in HPA-axis hyper-reactivity in adulthood, which can cause major depression. However, outcomes are dependent on later life stress; animals show normal brain structure and behavior unless they experience overwhelming stress events, in which case they will recall the traumatic memory and display affective disorders. Therefore, despite normal neural, hormonal, and/or behavioral responses, the early life stress still can induce adult affective disorders.

Recent epigenetic studies offer answers for this process. Emerging evidence has found that epigenetic processes are involved in early-life stress-mediating adult behavioral phenotypes. Epigenetic mechanisms enable cell-specific gene expressions and enable one genome to be programmed in many ways, resulting in diverse profiles of gene expression. DNA methylation, an enzymatic covalent modification of DNA, has been one of the principal epigenetic mechanisms investigated. Some early life events induce epigenetic changes for neuromodulator receptors or transporters, such as DNA methylation of adrenocorticotropic hormone (ACTH) or cortisol receptors, monoamine oxidase (MAO), or through miRNA changes. Both human and animal studies suggest that HPA-axis function may be altered through aberrant epigenetic modifications. These changes could affect the expression of certain genes under certain stressful conditions, which might induce the dysfunction of monoamines that are related to affective disorders.

In all, the idea that epigenetic mechanisms mediate the life-long effects of perinatal adversity has attractive potential implications for early detection, prevention, and intervention in mental health disorders. In this Research Topic, we would like to invite recent research studies on early life traumatic events with epigenetics involved in affective disorders. We encourage Original Research and Reviews about topics including, but not limited to, the following:
1. Early life stress-induced epigenetics, such as miRNA changes and methylation of DNA sequences of MAO-related proteins.
2. Epigenetic changes resulting in or related to adult affective disorders such as depression and anxiety, including epigenetic changes related to dopamine or serotonin receptors, to BDNF and/or GDNF, and to PKA or PKB signaling pathways.
3. Intervention methods to deal with early life epigenetic effects.

Keywords: early life stress, epigenetic effects, depression

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