Epidemiological and clinical studies have shown that children exposed to adverse experiences are at increased risk for the development of depression, anxiety disorders, and posttraumatic stress disorder (PTSD). A history of child abuse and maltreatment increases the likelihood of being subsequently exposed to traumatic events or of developing PTSD as an adult. The brain is highly plastic during early life and encodes acquired information into lasting memories that normally subserve adaptation. Translational studies in rodents showed that enduring sensitization of neuronal and neuroendocrine circuits in response to early life adversity are likely risk factors of life time vulnerability to stress. Hereby, the hypothalamic-pituitary-adrenal (HPA) axis integrates cognitive, behavioral, and emotional responses to early-life stress and can be epigenetically programed during sensitive windows of development. Epigenetic mechanisms, comprising reciprocal regulation of chromatin structure and DNA methylation, are important to establish and maintain sustained, yet potentially reversible, changes in gene transcription. The relevance of these findings for the development of PTSD requires further studies in humans where experience-dependent epigenetic programing can additionally depend on genetic variation in the underlying substrates which may protect from or advance disease development. Overall, identification of early-life stress-associated epigenetic risk markers informing on previous stress history can help to advance early diagnosis, personalized prevention, and timely therapeutic interventions, thus reducing long-term social and health costs.
Keywords: PTDS, depression, early-life stress, HPA axis, epigenetic programing, epigenetic variation
Citation: Raabe FJ and Spengler D (2013) Epigenetic risk factors in PTSD and depression. Front. Psychiatry 4:80. doi: 10.3389/fpsyt.2013.00080
Received: 29 April 2013; Accepted: 22 July 2013;
Published online: 07 August 2013.
Edited by:Tania L. Roth, University of Delaware, USA
Reviewed by:Seema Bhatnagar, Children’s Hospital of Philadelphia, USA
Copyright: © 2013 Raabe and Spengler. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Dietmar Spengler, Molecular Neuroendocrinology, Max Planck Institute of Psychiatry, Kraepelinstr. 2-10, 80804 Munich, Germany e-mail: firstname.lastname@example.org