Recent experiments suggested that during the early stage of the AD, Aβ could enter the mitochondria to increase the generation of free radicals and induce oxidative stress [43]; the ROS burst was mainly the result of impaired axonal transport and energy dysfunction of mitochondria caused by an abnormally phosphorylated tau protein [44]; the high concentration of redox-active copper and iron is consistent with their catalytic action in Fenton chemistry to form reactive hydroxyl radicals which may cause damage to biomolecules in the brain, including DNA [8]. Here, MAPT is linked to Alzheimer disease.