Cell and animal studies in AD models as well as post-mortem examinations of patients, although not always matching perfectly, signify that the transcription of fusion-enhancers (OPA1, mitofusin (Mfn)1/2) is attenuated and the expression or activity of fission-modulators (dynamin-related protein 1 (Drp1), mitochondrial fission 1 protein (Fis1) and S-nitrosylated Fis1) are aberrantly elevated. Here, FIS1 is linked to Alzheimer disease.