In summary, during the course of AD, dysregulation of protein kinases and phosphatases leads to tau hyperphosphorylation; increased tau phosphorylation inhibits the phosphorylation of β-catenin with mechanisms involving direct acetylation of β-catenin by tau, or through substrate competition of tau and β-catenin for the kinases (such as GSK-3β). This evidence concerns the gene MAPT and Alzheimer disease.