In line with several cohort studies including the Rotterdam Study [28], which have shown that cholesterol-lowering medications in midlife were associated with a 50–70% lower risk of late-life development of AD [29], we hypothesized that the inhibition of extracellular PCSK9 by FDA-approved monoclonal antibodies might strengthen LRP1-mediated Aβ clearance and thus be a potential therapeutic approach to AD. Here, LRP1 is linked to Alzheimer disease.