Furthermore, in healthy carriers of the apolipoprotein E (ApoE ε4) polymorphism, linked to Aβ clearance and heightened risk for AD development, miR-153-3p was shown to be increased, leading to blockage of nuclear factor erythroid-2-related-factor-2 (Nrf2)-mediated proteasomal function and erythrocyte Aβ accumulation in plasma [81]. This evidence concerns the gene APOE and Alzheimer disease.