Several studies have confirmed that APP and Aβ are critically involved in mitochondrial dysfunction and neuronal damage responsible for the progression of AD [42]; in particular, Aβ binds to mitochondrial proteins, such as the mitochondrial fission protein dynamin-related protein 1 (Drp1) [43], the mitochondrial protein of the MOM VDAC [15], the proteins of the mitochondrial matrix Aβ-binding alcohol dehydrogenase (ABAD), and cyclophilin D (CypD) (see [15]). This evidence concerns the gene DNM1L and Alzheimer disease.