AD models based on APP (amyloid precursor protein) or Aβ overexpression, or Aβ exposure also show increasingly fragmented mitochondrial networks with higher total numbers of mitochondria and reduced mitochondrial length likely caused by a shift in mitochondrial fission/fusion dynamics (Ye et al., 2015; Hu et al., 2016; Martín-Maestro et al., 2017; Castellazzi et al., 2019). The gene discussed is APP; the disease is Alzheimer disease.