Kundakovic and colleagues find that activation of reelin and GAD67 genes correlated with a reduction in DNA methyltransferase activity and DNMT1 protein levels. Lee and colleagues (2006), report that procainamide is a specific inhibitor of DNMT1. Might we expect that procainamide might restore the reduced reelin and GAD67 protein levels which have been found to be reduced in post-mortem brains of schizophrenic patients?
Is there a reduced risk of schizophrenia for those taking procainamide for rhythm defects and what are the implications for the fact that some atypical antipsychotics as well as procainamide may prolong the QT interval? Has anyone noticed an improvement in clinical stage after commencement of procainamide?
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