Abstract

PTSD is a multigenic and multifactorial disorder occurring in the aftermath of significant trauma exposure. Recent GWAS have identified many high confidence loci as risk factors for PTSD, which have shed some light on impaired mechanisms. However, there are still fundamental gaps in our understanding of how these risk genes and pathways are interrelated in causing PTSD but are likely reflected in cell type-specific transcriptomic and epigenetic changes in the brain. Therefore, it is necessary to uncover the individual cell type contribution to the molecular pathology of PTSD.

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