BACE1 and Alzheimer disease: It simply augments the efficiency of BACE1 cleavage at the β′ site within iAβ and thus reduces the steady-state influx of AβPP-derived iAβ and lowers the rate of its accumulation; ultimately, it delays or prevents (within limits of the lifespan) the crossing of the T0 and/or T1 thresholds and, consequently, the occurrence of AD and AACD.