Deutsch
 
Benutzerhandbuch Datenschutzhinweis Impressum Kontakt
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Buchkapitel

Epigenetics in posttraumatic stress disorder.

MPG-Autoren
/persons/resource/persons173117

Rampp,  Carina
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

/persons/resource/persons80272

Binder,  Elisabeth B.
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

/persons/resource/persons173119

Provencal,  Nadine
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

Externe Ressourcen
Es sind keine Externen Ressourcen verfügbar
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Rampp, C., Binder, E. B., & Provencal, N. (2014). Epigenetics in posttraumatic stress disorder. In Progress in molecular biology and translational science (pp. 29-50). Amsterdam: Elsevier Inc. doi:10.1016/B978-0-12-800977-2.00002-4.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0027-79BE-C
Zusammenfassung
Reported exposure to traumatic event is relatively common within the general population (40-90%), but only a fraction of individuals will develop posttraumatic stress disorder (PTSD). Indeed, the lifetime prevalence of PTSD is estimated to range between 7% and 12%. The factors influencing risk or resilience to PTSD after exposure to traumatic events are likely both environmental, such as type, timing, and extent of trauma, and genetic. Recently, epigenetic mechanisms have been implicated in mediating altered risk for PTSD as they can reflect both genetic and environmental influences. In this chapter, we describe the accumulating evidences for epigenetic factors in PTSD highlighting the importance of sensitive periods as well as methodological aspects such as tissue availabilities for such studies. We describe studies using a candidate gene approach focusing mainly on key players in the stress hormone regulation that show epigenetic alterations both in humans and in animal models for PTSD. We also summarize the results of epigenome-wide studies reporting associations with PTSD. For the above, we focus on one epigenetic mechanism, DNA methylation, as it is so far the best studied for this disorder. Finally, we describe how epigenetic mechanisms could be responsible for the long-lasting effects of gene-environment interactions observed in PTSD.