APP and familial Alzheimer disease: Aspects of human pathology have been replicated in mouse strains, most prominently the formation of beta-amyloid plaques via transgenic over-expression of brain-specific mutant human amyloid-beta precursor protein (APP), presenilin-1 (PS1), and/or microtubule-associated protein tau (MAPT) bearing familial Alzheimer’s disease (FAD) mutations (Bilkei-Gorzo, 2014).