On the other hand, drugs reducing iAβ levels via its targeted degradation regardless of its origin (i.e., both AβPP-derived and produced independently of AβPP), such as the enhancers of iAβ-cleaving activities of BACE1 and BACE2, would be equally effective in treatment of both AACD-CI and AD-MCI [1,2,3] (further discussed below). Here, BACE2 is linked to Alzheimer disease.