Considering the detrimental effects of Aβ in Hebbian synaptic plasticity together with promising results in experiments employing a mouse model that expressed familial mutant APP in the absence of BACE1 (Cai et al., 2001; Luo et al., 2001; Roberds et al., 2001), pharmacologic inhibition of BACE1 has been tested as a potential treatment for the cognitive decline in AD (Yan and Vassar, 2014; Coimbra et al., 2018). Here, BACE1 is linked to Alzheimer disease.