Deeping on the abnormal mitochondrial dynamics in relation to Aβ oligomers in the AD brain samples, Manczak et al. succeeded in the seminal demonstration that Drp1 and Fis1 increase with AD pathology evolution and that monomeric and oligomerc Aβs interact with the pro-fission protein Drp1 in both human AD and AβPP/PS1 transgenic mouse-derived samples, which may ultimately translate in the AD characteristic exaggerated mitochondrial fragmentation and neuronal demise (237). This evidence concerns the gene APP and Alzheimer disease.