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Genetic risk for psychiatric and neurodevelopmental disorders, including schizophrenia, autism spectrum disorder, and bipolar disorder, converges on synaptic biology. This convergence extends beyond static synaptic structures to the dynamic, activity-dependent molecular systems. We review how genetic risk variants disrupt post-transcriptional control by RNA-binding proteins, local translation and its machinery, and effectors of synaptic plasticity mechanisms. These disruptions impair neurocircuits in context-dependent manners shaped by developmental stage, cell type, and subcellular compartment. Understanding this multilayered convergence is key for translating genetic discoveries into therapeutic advances.
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Tamušauskaitė et al. (2026) studied this question.
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