GSK3B and Alzheimer disease: Hence, the truncation of GSK-3β is highly and positively correlated with tau phosphorylation at many sites in human brains, indicating increased tau phosphorylation in AD brain may result from increased GSK-3β kinase activity caused by its C-terminal truncation by calpain I. Activation of calpains might also involve truncation and activation or inhibition of other tau protein kinases or phosphatses and directly or indirectly affect tau phosphorylation.