APP and Alzheimer disease: Excessive mitochondrial fission and its deleterious effect were consistently demonstrated in cell models of AD in vitro, where overexpression of APP or Aβ treatment induces profound mitochondrial fragmentation, ultrastructural deficits, and altered distribution in neuronal cultures [15,16,17,18,21,22], which are likely causally involved in Aβ-induced synaptic abnormalities in hippocampal neurons.