Cholesterol is a key structural component of the brain, and cholesterol transport and distribution within the central nervous system CNS is mediated by a lipid metabolic cycle that includes generation of apolipoproteins as lipid carriers, lipidation by cholesterol and phospholipid transporters, enzyme remodeling of these particles and their receptor-mediated uptake and turnover in cells. It is becoming increasingly appreciated that "lzheimer's Disease "D patients often have comorbid conditions such as cardiovascular disease, type II diabetes mellitus, or hypertension, each of which can greatly affect lipoprotein metabolism, especially at the vessel wall and thereby possibly contribute to "D pathogenesis. Here we review the known biology of lipids and lipoproteins in the CNS and discuss how alterations in lipid metabolism may impact "D pathogenesis. "polipoprotein E APOE is the best established genetic risk factor for "D and the major apolipoprotein expressed in the brain. In addition, genome-wide association studies GW"S have identified several other genes associated with "D risk that function in lipid or lipoprotein metabolism, including clusterin CLU , "TP binding cassette ""C transporter " ABCA7 , and apoE receptors. Understanding how lipid/lipoprotein metabolism in the brain and body affect cognitive function may therefore offer new insights in developing more effective therapeutic approaches for dementia.