The findings are important, says William A. Banks, M.D., a Saint Louis University professor and the lead author of the article, because they give us a new approach for treating Alzheimer's disease.
"It's going to be a big piece to solving the Alzheimer's disease puzzle," says Dr. Banks, a professor of geriatrics in the department of internal medicine and professor of pharmacological science at Saint Louis University School of Medicine. "If one could reverse the transport deficit problem, the system should be able to pump the protein out again. The impaired transporter problem may be an easier therapeutic target."
Normally, amyloid beta protein, the protein thought to cause Alzheimer's disease, leaves the brain and crosses the blood brain barrier, which is a wall of blood vessels that feed the brain and regulate the entry and exit of brain chemicals. But in persons with Alzheimer's disease, amyloid beta protein becomes blocked in the brain and can't make it across the blood brain barrier. The more amyloid beta protein accumulates, the tougher it is for the blood brain barrier to move it out, and the more disabled a person becomes.
Because the transport deficit causes the amyloid beta protein to accumulate, scientists should focus on finding ways to destroy the protein with enzymes or pushing the protein across the blood brain barrier and out of the brain. Dr. Banks says fixing the system that transports amyloid beta protein across the blood brain barrier is "a viable therapeutic target."
"We need to find therapies to bring the transportation system back on line to pump the amyloid beta protein out of the brain," says Dr. Banks, who also is a staff physician at Veterans Affairs Medical Cente
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Contact: Nancy Solomon
solomonn@slu.edu
314-977-8017
Saint Louis University
6-Oct-2003