To date, commonly used animal models are transgenic mice that overexpress human genes associated with familial AD, leading to the formation of senile plaques of amyloid-β (Aβ) peptide (e.g., overexpression of human amyloid precursor protein (APP)) alone or with presenilin-1 (PSEN1) and neurofibrillary tangles of hyperphosphorylated tau protein (e.g., overexpression of human microtubule associated protein tau (MAPT)), two hallmarks of AD [2]. The gene discussed is APP; the disease is Alzheimer disease.