Division of Depression & Anxiety Disorders, McLean Hospital, Department of Psychiatry, Harvard Medical School, Oaks Building 328, Mailstop 212, 115 Mill Street, Belmont, MA, 02478-1064, USA.
Department of Psychiatry, Genetics and Genomic Sciences, Icahn School of Medicine, New York, NY, USA.
Curr Psychiatry Rep. 2018 Apr 5;20(5):30. doi: 10.1007/s11920-018-0898-7.
Following a life-threatening traumatic exposure, about 10% of those exposed are at considerable risk for developing posttraumatic stress disorder (PTSD), a severe and disabling syndrome characterized by uncontrollable intrusive memories, nightmares, avoidance behaviors, and hyperarousal in addition to impaired cognition and negative emotion symptoms. This review will explore recent genetic and epigenetic approaches to PTSD that explain some of the differential risk following trauma exposure.
A substantial portion of the variance explaining differential risk responses to trauma exposure may be explained by differential inherited and acquired genetic and epigenetic risk. This biological risk is complemented by alterations in the functional regulation of genes via environmentally induced epigenetic changes, including prior childhood and adult trauma exposure. This review will cover recent findings from large-scale genome-wide association studies as well as newer epigenome-wide studies. We will also discuss future "phenome-wide" studies utilizing electronic medical records as well as targeted genetic studies focusing on mechanistic ways in which specific genetic or epigenetic alterations regulate the biological risk for PTSD.
在经历危及生命的创伤性暴露后，约有 10%的暴露者面临患上创伤后应激障碍（PTSD）的高风险，这是一种严重且使人丧失能力的综合征，其特征是无法控制的侵入性记忆、噩梦、回避行为和过度警觉，此外还伴有认知和负性情绪症状受损。本篇综述将探讨 PTSD 的最新遗传和表观遗传方法，这些方法解释了创伤暴露后一些不同的风险。
解释创伤暴露后不同风险反应的差异可能部分归因于遗传和获得性的遗传和表观遗传风险的差异。这种生物风险通过环境诱导的表观遗传变化对基因的功能调节的改变来补充，包括先前的儿童和成人创伤暴露。本篇综述将涵盖来自大规模全基因组关联研究以及更新的全基因组表观遗传研究的最新发现。我们还将讨论未来利用电子病历的“表型全基因组”研究以及关注特定遗传或表观遗传改变如何调节 PTSD 生物学风险的靶向遗传研究。
