APOE and Alzheimer disease: A potential pathomechanism underlying this interaction between APOE ε4 and myelin is that microglial phagocytosis of cholesterol-rich lipid droplets from impaired myelin may lead to microglial senescence [71, 72] which is exacerbated by microglial APOE ε4 expression [66], rendering microglia less efficient in phagocyting core AD pathologies [67].