APP and Alzheimer disease: This model of mice carries the Swedish KM670/671 NL, Iberian I716F, and Arctic E693G mutations on the gene of amyloid-β precursor protein (APP) and displays Aβ plaque accumulation and neuroinflammation across age, reproducing neuropathological change in preclinical AD without artifacts caused by APP overexpression (Saito et al., 2014; Sasaguri et al., 2017).