ArticleGenome medicine2025
A multi-omic approach implicates novel protein dysregulation in post-traumatic stress disorder.
Article in Genome medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Advances in the Comprehensive Tree Shrew Brain Atlas.Biomolecules · 2026Review
- Alterations of microRNAs across human and mouse limbic brain areas: molecular mechanisms and biological processes involved in major depressive disorder.Neurobiology of stress · 2026Article
- A shared transcriptional network in the nucleus accumbens supports resilience to chronic stress across sex.bioRxiv : the preprint server for biology · 2026Article
- The novel ferroptosis-inducing molecule can inhibit the progression of BC by regulating the ubiquitination of UHRF1.Epigenomics · 2025Article
- Epigenetic modifications and transgenerational inheritance in women victims of violence (EWVV).Environmental epigenetics · 2025Review
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Authors and funding
23 authors.
Funding
Abstract
backgroundPost-traumatic stress disorder (PTSD) is a common and disabling psychiatric disorder. PTSD involves multiple brain regions and is often comorbid with other psychiatric disorders, such as major depressive disorder (MDD). Recent genome-wide association studies (GWASs) have identified many PTSD risk loci and transcriptomics studies of postmortem brain have found differentially expressed genes associated with PTSD cases. In this study, we integrated genome-wide measures across modalities to identify convergent molecular effects in the PTSD brain.
methodsWe performed tandem mass spectrometry (MS/MS) on a large cohort of donors (N = 66) in two prefrontal cortical areas, dorsolateral prefrontal cortex (DLPFC), and subgenual prefrontal cortex (sgPFC). We also coupled the proteomics data with transcriptomics and microRNA (miRNA) profiling from RNA-seq and small-RNA sequencing, respectively for the same cohort. Additionally, we utilized published GWAS results of multiple psychiatric disorders for integrative analysis.
resultsWe found differentially expressed proteins and co-expression protein modules disrupted by PTSD. Integrative analysis with transcriptomics and miRNA data from the same cohort pointed to hsa-mir-589 as a regulatory miRNA responsible for dysregulation of neuronal protein networks for PTSD, including the gamma-aminobutyric acid (GABA) vesicular transporter, SLC32A1. In addition, we identified significant enrichment of risk genes for other psychiatric disorders, such as autism spectrum disorder (ASD) and major depressive disorder (MDD) within PTSD protein co-expression modules, suggesting shared molecular pathology.
conclusionsWe integrated genome-wide measures of mRNA and miRNA expression and proteomics profiling from PTSD, MDD, and control (CON) brains to identify convergent and divergent molecular processes across genomic modalities. We substantially expand the number of differentially expressed genes and proteins in PTSD and identify downregulation of GABAergic processes in the PTSD proteome. This provides a novel framework for future studies integrating proteomic profiling with transcriptomics and non-coding RNAs in the human brain studies.
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