More specifically, prolonged mitochondrial fission and its deleterious effects are clearly illustrated in in vitro AD models: overexpression of amyloid precursor protein (APP) or Aβ treatment causes profound fragmentation and altered distribution of mitochondria, which likely trigger Aβ-induced synaptic defects in neuronal cultures (Wang et al., 2008, 2009a; Manczak et al., 2011). This evidence concerns the gene APP and Alzheimer disease.