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Chunk #3 — Introduction

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Genome-wide association analyses identify 95 risk loci and provide insights into the neurobiology of post-traumatic stress disorder.
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Furthermore, GWAS to date have had limited power to identify credible treatment candidates. PTSD is also known frequently to be comorbid and genetically correlated with other mental (e.g., major depressive disorder [MDD]; attention deficit hyperactivity disorder)14 and physical health conditions (e.g., cardiovascular disease; obesity)15–17, but studies to date are limited in their ability to parse shared and disorder-specific loci and link them to underlying biological systems. Importantly, prior GWAS are severely limited in generalizing their findings to non-European ancestries. Recent work on polygenic risk scores (PRS) in PTSD shows potential utility of these measures in research16–18, but also, vexingly, limited cross-population transferability. Without expansion to other ancestries, there is a risk that recent advances in PTSD genetics will result in the widening of research and treatment disparities. This inequity is particularly troubling in the US given the disproportionately high burden of trauma and PTSD faced by populations of African, Native, and Latin American origin19,20.