Multiple lines of evidence independently implicate PP2A in AD, among these are the observations that 1) PP2A expression and activity are reduced in brains from AD patients [5–8], 2) reducing PP2A activity in animal models results in AD-like pathology and cognitive deficits [9–15], 3) PP2A is the principal phosphatase for phosphorylated forms of tau linked to AD [16], and 4) pharmacological activation of PP2A reduces cognitive impairment and pathology in mouse tauopathy models [17–19]. This evidence concerns the gene MAPT and Alzheimer disease.