Polycomb Epigenetic Programs Contribute to Tic Disorder Pathophysiology Independently of Antipsychotic Drug Targets
This study demonstrates that tic disorder genetic liability is significantly enriched in Polycomb-regulated pathways governing neuronal identity, synaptic plasticity, and RNA processing—mechanisms distinct from antipsychotic drug targets—thereby offering a novel epigenetic rationale for the limitations of current treatments and identifying new targets for mechanism-based therapies.