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Possible involvement of epigenetic mechanisms in the neurobiology of PTSD
Pregelj, Peter ; Videtič Paska, Alja, 1980-
Exposure to a traumatic event is required for the diagnosis of posttraumatic stress disorder (PTSD). It was first suggested that PTSD represents a normative response to exposure to extreme stressors, ...but it soon became evident that only a minority of individuals who experience a traumatic event will develop the disorder. However, the relation between psychopathological events, the phenomenology of the trauma, and neurobiological changes related to PTSD is not totally understood. The symptoms of PTSD are believed to reflect stress-induced changes in neurobiological systems representing an inadequate adaptation of neurobiological systems to exposure to severe stressors. Attempts are made to relate different neurobiological changes to the specific features represented in PTSD. It is not clear whether certain neurobiological changes in PTSD reflect preexisting vulnerability or consequences of trauma exposure. It is known that early life environmental events have persisting effects on central nervous tissue structure and function, a phenomenon called "developmental programming." Further it is knownthat glucocorticoid hormone mediators may be involved in this process. Itwas suggested that changes in the glucocorticoid system are mediated by tissue-specific changes in gene expression. Recent studies suggest that epigenetic mechanisms may play an important role in the interplay between stress exposure and genetic vulnerability. In preclinical studies it was firstsuggested that epigenetic mechanisms may be involved in the modulation ofgene expression in response to stressful stimuli. Recently, epigenetic differences in a neuron-specific glucocorticoid receptor (NR3C1) promoter between postmortem hippocampus obtained from suicide victims with a history ofchildhood abuse and those from either suicide victims with no childhood abuse or controls were found, indicating the involvement of these mechanisms in human adaptation to stress. (Abstract truncated at 2000 characters)
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