Importantly, the correction of excessive mitochondrial fission and mitochondrial pathology by P110 was observed in fibroblasts from AD patients regardless of the form of AD (sporadic or familial), suggesting that a selective inhibitor Drp1/Fis1 interaction, such as P110, with may have a broad clinical use to halt or slow down the underlying neuronal degenerative process of AD. Here, DNM1L is linked to Alzheimer disease.