Increasing evidence suggested that an abnormal mitochondrial dynamics is likely involved in the mitochondrial structural damage and dysfunction in AD: several groups demonstrated that overexpression of familial AD-causing amyloid precursor protein (APP) mutants or exposure to soluble oligomeric Aβ caused changes in the expression of mitochondrial fission and fusion proteins and profound mitochondrial fragmentation in neuronal cells which led to ultrastructural damage to mitochondria and mitochondrial dysfunction along with neuronal deficits such as synaptic abnormalities in vitro [9–14]. Here, APP is linked to Alzheimer disease.