APP and familial Alzheimer disease: Both investigations used the 5XFAD mouse model, a preclinical transgenic model that overexpresses mutant human amyloid beta (A4) precursor protein 695 (APP) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) familial Alzheimer’s disease (FAD) mutations, as well as two FAD mutations, M146L and L286V of the human presenilin 1 [46].