Compelling evidence implicates oxidative stress in the pathophysiology of AD, promoting tau hyperphosphorylation and neurofibrillary pathology by inhibition of phosphatase 2A, which activates glycogen synthase kinase 3β (GSK3β) [24,25], and accumulation of Aβ by ROS-induced inhibition of the proteasomal system through impaired mammalian target of rapamycin (mTOR) signaling [26]. This evidence concerns the gene MAPT and Alzheimer disease.