Manczak et al. confirmed that Aβ co-localizes and interacts with Drp1 via immunoprecipitation and double-labeling immunofluorescence analyses of Aβ and Drp1 in the frontal cortex of AD patients and in the primary neurons of APP transgenic mice, which in turn causes excessive mitochondrial fission and leads to neuronal damage, and that this interaction is enhanced with the progression of AD [49]. Here, APP is linked to Alzheimer disease.