Although genetic mutations in AD account for a small proportion of all AD cases, most of our understanding of AD pathology and mechanisms have come from animal models with these genetic mutations, for example the J20 mouse (PDGFB-hAPPSwInd) harbours the more common APP mutation called the Swedish K670 N/M671L mutation as well as the Indiana V717F mutation, which both increase β-secretase activity [47, 48]. This evidence concerns the gene APP and Alzheimer disease.