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2005 Grant - Loeffler
Alterations in Complement Activation During Alzheimer's Disease Development
David Loeffler, D.V.M., Ph.D.
William Beaumont Hospital
Royal Oak, Michigan
2005 Investigator-Initiated Research Grant
Inflammation is a part of the body's response to disease or injury, but long-term inflammation may damage tissues. Inflammation may be a contributing factor to the damage that occurs to the brain in Alzheimer's disease. Although current anti-inflammatory treatments have not been found effective in treating Alzheimer's, a better understanding of inflammatory processes in Alzheimer's disease may lead to new anti-inflammatory treatment options.
David Loeffler, D.V.M., Ph.D., and colleagues are studying an inflammatory process called complement activation. They have observed that proteins produced early in this process promote the clearance of beta-amyloid, a protein fragment that may be a key toxic factor in Alzheimer's. They have also observed that increased production of these proteins may be associated with normal aging. However, full complement activation produces other proteins that appear to be toxic to cell membranes.
The investigators will study complement activation in mice that are genetically altered to develop an Alzheimer-like pathology and symptoms. By experimentally manipulating complement activation, they will be able to assess the significance of this process in the development and progression of Alzheimer's disease. Outcomes of the research may lead to the clinical investigation of currently available therapies as Alzheimer treatments or identify targets for new anti-inflammatory drugs.