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Findings provide proof-of-concept for the utility of pPGSs in psychiatric research, suggesting both genetic contributions to trauma exposure and GxE effects on psychosis risk, as well as supporting pathway-specific contributions beyond general polygenic risk.
CA was not consistently associated with hippocampal or amygdala volume alterations in PD and BD, and more consistent evidence emerged for reduced GMV in prefrontal regions, suggesting that neurobiological impact of CA may be more robustly captured at the cortical level.
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