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2007 Grant - Vitek
Novel Therapeutic Reduces Beta-Amyloid Deposition and Alzheimer Pathology
Michael Vitek, Ph.D.
Duke University Medical Center
Durham, North Carolina
2007 Investigator-Initiated Research Grant
Beta-amyloid is a protein fragment that may be a key factor in damaging cell-to-cell communication and causing the loss of brain cells in Alzheimer's disease. Beta-amyloid clumps together in stages, eventually forming amyloid plaques.
One of the risk factors for Alzheimer's disease is head trauma that has occurred earlier in life. Michael Vitek, Ph.D., and colleagues have devised a procedure to induce head trauma in mice genetically engineered to develop Alzheimer-like symptoms. This procedure does not break the skull. Dr. Vitek's team found that such head trauma leads to the production of beta-amyloid. Further studies identified a fragment of apolipoprotein-E, an Alzheimer-related protein, that can significantly prevent beta-amyloid production in the mice.
For this proposed grant, Dr. Vitek and colleagues will seek to confirm their earlier results by conducting a more thorough study with their mice. They will generate severe brain inflammation in the animals through head trauma or injection of bacterial toxin. They will then treat some of the mice with either the apolipoprotein-E fragment or an antibiotic called minocycline. Finally, the researchers will analyze whether these treatments prevented beta-amyloid deposition in the mice or improved the animals' cognitive or behavioral performance. Results from this study could lead to novel therapies for preventing Alzheimer's disease in people who have experienced prior head trauma.