Research Letter: PTSD has shared polygenic contributions with bipolar disorder and schizophrenia in women

Twin studies have demonstrated overlap between genetic contributions to post-traumatic stress disorder (PTSD) and other psychiatric disorders (Kremen et al. 2012). These findings have prompted interest in examining shared genetic risk between PTSD and other psychopathology at the molecular level. Wi...

Full description

Saved in:
Bibliographic Details
Published in:Psychological medicine Vol. 46; no. 3; pp. 669 - 671
Main Authors: Sumner, J. A., Duncan, L., Ratanatharathorn, A., Roberts, A. L., Koenen, K. C.
Format: Journal Article
Language:English
Published: Cambridge Cambridge University Press 01.02.2016
Subjects:
ISSN:0033-2917, 1469-8978
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Twin studies have demonstrated overlap between genetic contributions to post-traumatic stress disorder (PTSD) and other psychiatric disorders (Kremen et al. 2012). These findings have prompted interest in examining shared genetic risk between PTSD and other psychopathology at the molecular level. With genome-wide association studies (GWAS) and collaborative consortia-based efforts, replicable risk variants have been identified for schizophrenia and bipolar disorder (Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013; Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014). Analyses of genetic loci in aggregate (polygenic effects; Purcell et al. 2009) have demonstrated shared genetic risk between schizophrenia, bipolar disorder, and major depressive disorder (MDD), with greatest overlap for schizophrenia and bipolar disorder (Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013). Using 3742 candidate single nucleotide polymorphisms (SNPs), an initial polygenic analysis of PTSD by our group (Solovieff et al. 2014) suggested overlap in genetic risk for bipolar disorder and PTSD in European American (EA) women that was replicated in a male EA sample with genome-wide data (Nievergelt et al. 2015).
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ISSN:0033-2917
1469-8978
DOI:10.1017/S0033291715002135