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2005 Grant - Husemann
Role of Astrocytes in Beta-Amyloid Metabolism
Jens Husemann, M.D.
Columbia University Medical Center
New York, New York
2005 Investigator-Initiated Research Grant
A key feature of Alzheimer's disease is the aggregation, or clumping together of the beta-amyloid protein fragment. Beta-amyloid is a key suspect in the processes that damage cell-to-cell communication and the loss of cells. Studies have shown that a relatively early change in the Alzheimer brain is the accumulation of "helper" cells called astrocytes.
In preliminary studies, Jens Husemann, M.D., determined that astrocytes bind to, internalize and break down beta-amyloid, suggesting that astrocytes may play an important role in the clearance of beta-amyloid. However, the astrocyte clusters appear to be incapable of removing beta-amyloid deposits in the Alzheimer brain. This raises the possibility that a failure in astrocyte function may play a role in the aggregation of beta-amyloid.
The aim of Dr. Husemann's current research is to evaluate the potential role of astrocytes in clearing beta-amyloid deposits. The researchers will conduct experiments to (1) characterize the properties of astrocytes that enable them to degrade beta-amyloid, (2) determine what other factors may influence the ability of astrocytes to degrade beta-amyloid and (3) assess differences in astrocytes that may be associated with aging or location in the brain.
A better understanding of astrocyte function may suggest new strategies for developing Alzheimer's disease treatments.