Risk of Post-Traumatic Stress Disorder is partially genetic
The largest genetic study of individuals with PTSD reveals six regions in the human genome, which influence the risk of developing the disorder.
Post-traumatic stress disorder impairs the life of 3.6% of the world population. PTSD emerges after a traumatic experience and can last for several years – but people differ in the timing, severity, and even in the presence of the disorder.
In an international effort to dissect foundations of PTSD, scientists analyzed genomes (in a GWAS form) of over 30,000 cases and 170,000 healthy individuals. Investigated group included people of European, African, and Native American ancestry.
Three regions influencing the risk of PTSD were common for all individuals: near gene ZDHHC14, close to gene PARK2, and near a cluster of LINC02335, MIR5007, TUC338.
Moreover, data between ancestries pointed to additional – local – regions. European males were found to be influenced by variants near gene ZNF813, and near genes KAZN and TMEM51-AS1. African males depended on a region near genes LINC02571 and HLA-B.
Discovered genes contribute to neurobiological metabolism, including dopamine governance. Some of the genes were previously linked to other psychiatric disorders, such as Parkinson’s disease.
Our genetic findings squarely place PTSD among the other psychiatric disorders in terms of heritability and genetic relationship with other disorders.From the publication
Using vast genomic data, scientists developed a polygenic risk score for PTSD risk. People most genetically vulnerable were predicted to have a 40% higher risk of developing PTSD after exposure to trauma.
New genetic details about PTSD could drive the development of new biological treatments, as well as novel methods of prevention.
Publication: Nievergelt, C. M., Maihofer, A. X., Klengel, T., Atkinson, E. G., Chen, C. Y., Choi, K. W., … & Levey, D. F. (2019). International meta-analysis of PTSD genome-wide association studies identifies sex-and ancestry-specific genetic risk loci. Nature Communications, 10(1), 1-16. Doi:10.1038/s41467-019-12576-w.