Role of Abeta in brain blood vessel dysfunction

Gregory Zipfel, MD
Washington University (St. Louis, MO)
Year Awarded:
2007
Grant Duration:
April 1, 2007 to March 31, 2009
Disease:
Alzheimer's Disease
Award Amount:
$150,000
Grant Reference ID:
A2007352
Award Type:
Pilot
Award Region:
US Midwestern

Immunotherapy for Cerebral Amyloid Angiopathy

Summary

The long-term goals of this research are to determine how CAA causes stroke and dementia and to discover effective treatments for CAA and AD.

Details

Cerebral amyloid angiopathy (CAA) involves deposition of a protein called amyloid-ß (Aß) into brain blood vessels. It is almost universally found in patients with Alzheimer's Disease (AD). CAA can lead to stroke and dementia, likely by causing blood vessel dysfunction and lowering blood flow to the brain. We hypothesize that treating CAA with an anti-Aß antibody (an antibody directed against the Aß protein) will improve blood vessel function and blood flow to the brain. If true, this would prove that Aß deposits are the reason why CAA leads to blood vessel dysfunction and reduced brain blood flow. It would also mean that these antibodies may represent a new treatment for CAA and AD. The specific aims of this project are as follows: 1. To determine whether 'preventive' anti-Aß antibodies prevent or substantially reduce blood vessel dysfunction and reductions in brain blood flow caused by CAA. 2. To determine whether 'therapeutic' anti-Aß therapy decreases the severity of CAA, and if so, will such therapy reduce blood vessel dysfunction and reductions in brain blood flow caused by CAA. The long-term goals of this research are to determine how CAA causes stroke and dementia and to discover effective treatments for CAA and AD.
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