Figure 2: Propose model of LDL cholesterol-induced amyloidogenic processing of AβPP Elevated plasma LDL cholesterol, once it enters brain, can be internalized by neurons via receptor-mediated endocytosis. The LDL cholesterol internalization process promotes AβPP internalization. Increased apoB-containing LDL-cholesterol can lead to cholesterol accumulation in endolysosomes thus elevating endolysosome pH and impairing endolysosome function. Elevation of endolysosome pH can lead to increased BACE-1 protein levels and enhanced BACE-1 activity that leads to amyloidogenic processing of APP, and can reduce cathepsin activity thus impairing Aβ degradation in lysosomes.