Hyperphosphorylation of tau at several abnormal hyperphosphorylation sites, as seen in AD brain, can be observed in OA-treated brain slices [50], as it has been suggested that the decrease in PP2A activity in AD brain may cause the activation of ERK1/2, MEK1/2, and p70 S6 kinase, and the abnormal hyperphosphorylation of tau, both via increased phosphorylation and decreased dephosphorylation. Here, MAPK3 is linked to Alzheimer disease.