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2006 Grant - Deane
Regulation of Amyloid-Beta Brain Efflux by Copper
Rashid Deane, Ph.D.
University of Rochester
Rochester, New York
2006 Investigator-Initiated Research Grant
The beta-amyloid protein fragment accumulates at an abnormal rate in the Alzheimer brain, either because beta-amyloid is overproduced, not cleared from the brain efficiently, or both. Beta-amyloid is believed to be a major factor in the break down of cell-to-cell communication and loss of brain cells.
Studies have shown that low-density lipoprotein receptor-related protein 1 (LRP) helps clear beta-amyloid from the brain. It transports the protein fragment across the blood-brain barrier, the brain's defense against foreign substances in the bloodstream. Once beta-amyloid is ushered into blood vessels, the bloodstream takes it away.
Copper has long been suspect in Alzheimer pathology because it helps with the assembly of abnormal beta-amyloid structures in the brain. Recent studies have shown that certain levels of copper in the brain may also result in reduced levels of LRP.
Rashid Deane, Ph.D., and colleagues will study the role of copper in LRP-mediated clearance of beta-amyloid in the brains of mice and will study the impact of copper on beta-amyloid-LRP interactions in cell cultures. A better characterization of the role of copper in beta-amyloid clearance may suggest new therapeutic strategies for further investigation.