PRKN and Alzheimer disease: It was demonstrated that APP-CTF accumulation in the mitochondria of various AD study models caused the increased recruitment of PINK1/Parkin to mitochondria, the greater conversion of LC3, the accumulation of LC3-II, the non-degradation of the p62 substrate, enhanced levels of membrane and matrix mitochondrial proteins, and the deficient fusion of mitochondria with lysosomes [140].