SynthesisNeurobiology of aging2026
Post-traumatic stress disorder moderates the association between BrainAge acceleration and GrimAge acceleration.
Synthesis in Neurobiology of aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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21 authors.
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Abstract
Individuals with post-traumatic stress disorder (PTSD) are at higher risk for age-related physical comorbidities, such as cardiovascular disorders, and exhibit accelerated epigenetic and brain aging. The present study examined PTSD as a moderator of the association between DNA methylation (DNAm)-based systemic aging (GrimAge, PhenoAge) and brain aging, indexed by MRI-based and DNAm-derived BrainAge estimates, in 174 lifetime PTSD cases and 138 trauma-exposed controls from four cohorts. Peripheral DNAm assayed with the MethylationEPIC BeadChip was used to calculate epigenetic age acceleration (EAA), using multiple clocks (GrimAge, PC GrimAge, PC PhenoAge), and DNAm-based BrainAge acceleration. Neuroimaging-derived BrainAge estimates were calculated with T1-weighted MRI scans that were processed using FreeSurfer v5.3 and run on BrainageR. Meta-analysis of the four cohorts examined the interactions between lifetime PTSD and EAA on BrainAge acceleration. EAA measures were intercorrelated (0.43 < r
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