Abstract
Stressor exposure during early life has the potential to increase an individual’s susceptibility to a number of neuropsychiatric conditions such as mood and anxiety disorders and schizophrenia in adulthood. This occurs in part due to the dysfunctional stress axis that persists following early adversity impairing stress responsivity across life. The mechanisms underlying the prolonged nature of this vulnerability remain to be established. Alterations in the epigenetic signature of genes involved in stress responsivity may represent one of the neurobiological mechanisms. The overall aim of this review is to provide current evidence demonstrating changes in the epigenetic signature of candidate gene(s) in response to early environmental adversity. More specifically, this review analyses the epigenetic signatures of postnatal adversity such as childhood abuse or maltreatment and later-life psychopathology in human and animal models of early life stress. The results of this review shows that focus to date has been on genes involved in the regulation of hypothalamic-pituitary-adrenal (HPA) axis and its correlation to subsequent neurobiology, for example, the role of glucocorticoid receptor gene. However, epigenetic changes in other candidate genes such as brain-derived neurotrophic factor (BDNF) and serotonin transporter are also implicated in early life stress (ELS) and susceptibility to adult psychiatric disorders. DNA methylation is the predominantly studied epigenetic mark followed by histone modifications specifically acetylation and methylation. Further, these epigenetic changes are cell/tissue-specific in regulating expression of genes, providing potential biomarkers for understanding the trajectory of early stress-induced susceptibility to adult psychiatric disorders.
Highlights
Life stress (ELS) encompasses childhood abuse, neglect, poverty and parental illness, alongside a multitude of other stressors
The HPA axis involves the release, following a stressor, of the neuropeptide corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) from the paraventricular nucleus (PVN) of the hypothalamus. These bind to their specific receptors in the anterior pituitary that stimulate the release of adrenocorticotrophic hormone (ACTH) which stimulates the adrenal cortex to release glucocorticoid (GC) hormones, cortisol in human and corticosterone in rodents
The results suggested significant association of depression induced by maternally deprived (MD) to Bdnf and miR-16 levels but not the late-life stressors such as the chronic unpredictable stress in adulthood (CUPS) emphasising the role of Early life stress (ELS)-induced epigenetic alterations
Summary
Life stress (ELS) encompasses childhood abuse, neglect, poverty and parental illness, alongside a multitude of other stressors. The HPA axis involves the release, following a stressor, of the neuropeptide corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) from the paraventricular nucleus (PVN) of the hypothalamus These bind to their specific receptors (the CRHR1 and V1b receptors) in the anterior pituitary that stimulate the release of adrenocorticotrophic hormone (ACTH) which stimulates the adrenal cortex to release glucocorticoid (GC) hormones, cortisol in human and corticosterone in rodents. The role of candidate genes outside of the HPA axis Candidate genes such as the serotonin transporter SLC6A4 and BDNF have been highly implicated in stress response and in increased risk for psychiatric disorders [28,29,30,31,32].
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