It also posits that a single, once-in-a-lifetime-only, administration of iAβ depletion treatment via transient activation of BACE1 and/or BACE2, exploiting their Aβ-cleaving activities, or by any other suitable means, would not only prevent AD and AACD but would also be effective at the symptomatic stages of both disorders. Here, BACE2 is linked to Alzheimer disease.