Nikolaos P Daskalakis1, Chuda M Rijal1, Christopher King1, Laura M Huckins2, Kerry J Ressler3. 1. 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. 2. Department of Psychiatry, Genetics and Genomic Sciences, Icahn School of Medicine, New York, NY, USA. 3. 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. kressler@mclean.harvard.edu.
Abstract
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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.
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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.
Entities:
Keywords:
DNA methylation; Epigenetics; GWAS; Genetics; PTSD
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