Under cellular stress conditions, particularly in AD, changes in mitochondrial morphology is shifted towards immoderately enhanced fission, through changes in the expression of mitochondrial fission proteins, namely dynamin-like protein 1 (Drp1) and mitochondrial fission protein-1 (Fis1), and fusion proteins, namely mitofusin 1/2 (MFN1/2) and optic atrophy 1 protein (OPA1) [66,76]. Here, DNM1L is linked to Alzheimer disease.