Glycogen synthase kinase-3 beta, beta-catenin, and tau in postmortem bipolar brain

Therapeutic concentrations of the anti-bipolar drug lithium inhibit the act ivity of glycogen synthase kinase-3 beta, which raises the possibility that this enzyme and its substrates may be altered in the brain of subjects wit h bipolar disorder. Therefore, in prefrontal cortical samples from subjects with bipolar disorder and age-matched control subjects, we examined the le vels of glycogen synthase kinase 3 beta and of two proteins modified by it, beta-catenin and the microtubule associated protein tau. There were no sig nificant differences between subject groups among these measurements, but t here was a tendency for the tau isoform profile to be modified in bipolar t issue. Thus, while there are no differences between bipolars and controls i n prefrontal cortical levels of glycogen synthase kinase-3 beta, beta-caten in, or tau, tau isoform levels or phosphorylation states may be modified in bipolar disorder.