MFN1 and Alzheimer disease: Electron and confocal microscopy, gene expression analysis, and biochemical methods have helped to demonstrate that neurons from samples treated with Aβ alone exhibit increased expression of DRP1 and Fis1 (fission genes) and decreased expression of Mfn1, Mfn2, and Opa1 (fusion genes), which suggests abnormal mitochondrial dynamics in brain neurons in AD patients [31].