The scenario depicted in Figure 12 considers the prevention of symptomatic Alzheimer’s disease by ACH2.0 drugs, i.e., by the transient depletion of iAβ through its targeted degradation by activators of intra-iAβ-cleaving capabilities of BACE1 and/or BACE2 or by any other suitable agent. This evidence concerns the gene BACE1 and Alzheimer disease.