Decreased expression of the low-density lipoprotein receptor-related protein 1 (LRP-1) and P-glycoprotein (P-gp), as well as upregulation of the receptor for advanced glycation end products (RAGE), are mechanisms reported to be changed in AD patients, leading to Aβ accumulation in the brain [2, 3]. This evidence concerns the gene LRP1 and Alzheimer disease.