Most importantly, inhibiting the DRP1-FIS1 interaction corrects these mitochondrial impairments, reduces in the 5xFAD mice AD model (that overexpress human APP and PS1 transgenes with a total of five AD-linked mutations) cognitive defects, Aβ40 and Aβ42 levels, and oxidative stress, and increases ATP levels [80]. Here, FIS1 is linked to Alzheimer disease.