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2009 Grants - Reddy
Neuroprotection and Alzheimer's Disease
P. Hemachandra Reddy, Ph.D.
Oregon Health and Science University
2009 New Investigator Research Grant
Beta-amyloid, a protein fragment at the focus of Alzheimer research, is known to be toxic to nerve cells. However, the mechanisms of toxicity are not well understood. During the early stages of Alzheimer's disease, cells are known to exhibit damage to mitochondria, specialized organelles that are commonly known as the cell's energy plant.
P. Hemachandra Reddy, Ph.D. and colleagues are studying whether beta-amyloid damages mitochondria. Using mice that had been genetically altered to express high levels of beta-amyloid, as well as autopsy specimens of humans who had died of Alzheimer's disease, the researchers found that certain forms of beta-amyloid were found in the mitochondrial membrane of nerve cells. Furthermore, beta-amyloid disrupted numerous mitochondrial functions, interfering with cellular energy production and leading to cell death. Other researchers have also found evidence that beta-amyloid-induced damage to nerve cells in culture can be prevented by drugs that preserve mitochondrial function.
Dr. Reddy and colleagues are planning to extend their studies to determine if drugs that preserve mitochondrial function in cultured nerve cells can protect brain function in mice with Alzheimer-like pathology. They will use biochemical and imaging techniques to observe mitochondrial function as well as nerve cell function during treatment with these drugs. The researchers will also determine if such treatment preserves cognitive function in mice with Alzheimer pathology. These studies will provide initial information about the potential efficacy of a candidate drug treatment for slowing or halting the progression of Alzheimer's disease.