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2008 Grants - Hindupur
Mechanisms Underlying the Biogenesis of Mitochondrial Abeta
Anand Hindupur, Ph.D.
University of Pennsylvania
2008 Investigator-Initiated Research Grant
Beta-amyloid, a protein fragment, tends to accumulate in the brains of people with Alzheimer's disease. Beta-amyloid is clipped from its parent molecule, amyloid precursor protein (APP). Growing research indicates that beta-amyloid may cause disease by disrupting the function of mitochondria. Mitochondria are cellular structures that use oxygen and nutrients to produce energy for a cell. However, scientists do not know the exact role that beta-amyloid plays in mitochondrial dysfunction.
In previous research, Anand Hindupur, Ph.D., and colleagues found that mitochondria-associated beta-amyloid is produced from a certain type of APP. This APP appears to have a distinctive shape. The researchers also found that mitochondrial beta-amyloid is first clipped from its APP variant and then transported from the parent molecule to the mitochondria.
For this proposed study, Dr. Hindupur's team will use cultured cells to confirm their earlier results. They hope to learn more about how enzymes cut mitochondrial beta-amyloid from APP. In addition, the team plans to further analyze how this type of beta-amyloid is transported to mitochondria, and how it may impair mitochondrial functions.
The results of Dr. Hindupur's study could lead to a better understanding of beta-amyloid's role in the development of Alzheimer's disease. Such knowledge could lead to the development of novel treatments to prevent or slow the progression of Alzheimer's.