APP and Senile plaques: Furthermore, we selected knock‐in mice with KM670/671NL, E693G, and I716F mutations in the amyloid precursor protein (AppNL‐G‐F mice; APP‐KI mice) as a model for the preclinical stage of AD, which exhibits severe accumulation of amyloid β (Aβ) (Saito et al., 2014; Sasaguri et al., 2017), a major component of senile plaques, in the mouse brain.