Recent Genetics and Epigenetics Approaches to PTSD

被引:88
作者
Daskalakis, Nikolaos P. [1 ]
Rijal, Chuda M. [1 ]
King, Christopher [1 ]
Huckins, Laura M. [2 ]
Ressler, Kerry J. [1 ]
机构
[1] Harvard Med Sch, McLean Hosp, Dept Psychiat, Div Depress & Anxiety Disorders, Oaks Bldg 328,Mailstop 212,115 Mill St, Belmont, MA 02478 USA
[2] Icahn Sch Med, Dept Psychiat Genet & Genom Sci, New York, NY USA
关键词
PTSD; Genetics; Epigenetics; GWAS; DNA methylation; POSTTRAUMATIC-STRESS-DISORDER; GENOME-WIDE ASSOCIATION; NATIONAL COMORBIDITY SURVEY; C-REACTIVE PROTEIN; DNA METHYLATION; PSYCHIATRIC GENETICS; ENDOPHENOTYPE CONCEPT; DISEASE ASSOCIATIONS; TRAUMA EXPOSURE; RISK;
D O I
10.1007/s11920-018-0898-7
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
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.
引用
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页数:12
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