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2010 Grants - Yan
Blocking RTN3 Aggregation for Improving Cognitive Function
Riqiang Yan, Ph.D.
Cleveland Clinic Foundation
2010 Novel Pharmacological Strategies to Prevent Alzheimer's Disease
RTN3 is a protein that was initially found to inhibit the activity of an enzyme that produces beta-amyloid. This finding was significant because beta-amyloid is a protein fragment that is toxic to nerve cells and which aggregates to form amyloid plaque, one of the characteristic features of Alzheimer pathology. Recent studies have found, however, that RTN3 also aggregates and accumulates in regions of nerve cells that degenerate in Alzheimer's disease. Evidence suggests that aggregation of RTN3 makes it unavailable to inhibit the production of beta-amyloid, suggesting that aggregation of RTN3 may be one of the early steps in the initiation of Alzheimer's disease.
Riqiang Yan, Ph.D., and colleagues have proposed to study the role of RTN3 in the progression of Alzheimer pathology. They plan to create a strain of mice genetically altered to express lack of RTN3. Previous studies have shown that such mice will develop Alzheimer pathology at a very young age. The researchers will perform detailed studies of brain pathology in these animals to determine if lack of RTN3 causes degeneration of nerve cells such as that observed in animals with aggregated RTN3. Dr. Yan's team will then examine whether similar pathological changes occur in the brains of humans. These studies will help determine whether an inhibitor of RTN3 aggregation should be studied as a potential drug therapy in early stages of Alzheimer's disease.