Inflammation increases amyloid plaque deposition in Alzheimer's disease. Levels of inflammation are inversely correlated with the levels of high density lipoprotein (HDL) and apolipoprotein A-1 (Apo A-1), which is the major protein component of plasma HDL. Low levels of serum HDL and Apo A-1 are also correlated with an increased risk for AD. In this proposal the investigator proposes that agents which enhance levels of HDL and Apo A-l will inhibit amyloid plaque deposition. The investigator has developed an Apo A-1 peptide mimetic which has been investigated for its beneficial effects on atherosclerosis. Oral administration of this peptide has been shown to inhibit atherosclerosis in various animal models. In this proposal the investigator will now assess the effects of oral administration of the Apo A-1 mimetic in combination with cholesterol lowering statins to determine whether this therapy improves the cognitive function and brain amyloid deposition in an Alzheimer's mouse model.