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2007 Grant - Levy
Cystatin C-Derived Peptides as Inhibitors of Beta-Amyloid Aggregation
Efrat Levy, Ph.D.
Nathan S. Kline Institute for Psychiatric Research
Orangeburg, New York
2007 Investigator-Initiated Research Grant
The protein fragment beta-amyloid is suspected of damaging cell-to-cell communication and causing cell death in Alzheimer's disease. Beta-amyloid tends to accumulate into clumps called plaques. Many Alzheimer studies have focused on developing therapies that either hinder the production of beta-amyloid or promote its clearance from the brain.
Efrat Levy, Ph.D., and colleagues are studying ways to keep beta-amyloid in a soluble form that does not accumulate into plaques or other harmful aggregates. Recent research has indicated that an enzyme called cystatin C may play a role in inhibiting plaque development. Dr. Levy's team has found that when cystatin C binds to beta-amyloid, this binding inhibits the accumulation of beta-amyloid in cell cultures and in mice genetically engineered to develop Alzheimer-like symptoms. The team also has found that cystatin C helps protect nerve cells in cultures where toxic beta-amyloid clumps are present.
For their proposed grant, Dr. Levy and colleagues will conduct a detailed study of the structure of cystatin C. They hope to find the precise region of the enzyme that binds to beta-amyloid and inhibits plaque formation. They then will conduct a more extensive study with mice to confirm the ability of cystatin C to control beta-amyloid accumulation. Results from this study could lead to the development of cystatin-based drug therapies for Alzheimer's disease.