We have previously demonstrated an interaction between fibrinogen, the pro-inflammatory protein component of blood clots, and Abeta, the principal component of amyloid plaques that characterize Alzheimer's disease. Abeta alters the structure of fibrin blood clots and makes them more resistant to degradation, which may contribute to the brain inflammation and disordered cerebral vasculature found in Alzheimer's disease patients. We propose to find a drug that will inhibit the interaction between Abeta and fibrinogen. We believe that such a drug will help normalize the blood clotting system and cerebral blood flow in patients, thereby promoting neuronal survival and slowing or halting the progression of Alzheimer's disease.