Manczak et al. reported that in APP transgenic AD model mice, expression of the mitochondrial fission genes Drp1 and Fis1 increased, expression of mitochondrial fusion genes Mfn1, Mfn2, Opa1 and Tomm40 decreased, and that Drp1 interacted with the Aβ monomer and oligomer, suggesting that increased production of Aβ and the interaction of Aβ with Drp1 are crucial factors in mitochondrial fragmentation, abnormal mitochondrial dynamics and synaptic damage [31]. This evidence concerns the gene APP and Alzheimer disease.