To address whether the BACE1 elevation observed in AD brain is merely a passive end product of advanced neurodegeneration and cell death or whether it is actively involved in disease progression, we examined BACE1 levels in two Tg models of AD [143], namely the 5XFAD mouse [60] that develops amyloid plaques at young ages and exhibits significant neuronal loss, and the Tg2576 mouse [52], which develops plaques at older ages and does not show neuronal death. This evidence concerns the gene BACE1 and Alzheimer disease.