Dysfunctional mitochondria produce higher levels of reactive oxygen species, and the interactions of Aβ and P-tau with the mitochondrial proteins Drp1, VDAC, CypD, ABAD, PINK1, and Parkin enhance mitochondrial fragmentation and reduce mitophagy, leading to defective mitochondria in AD. The gene discussed is PRKN; the disease is Alzheimer disease.