Studies have shown that mitophagy in AD patients and AD models is significantly reduced [8,9]; Aβ and P-Tau hinder the PINK1–Parkin pathway, increase the production of ROS, destroy the mitochondrial membrane, and aggravate the mitochondrial structural and functional abnormalities [10,11], suggesting that the neuropathology of AD forms a vicious cycle with mitophagy disorder. This evidence concerns the gene PRKN and Alzheimer disease.