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More Insight Into Alzheimer's Disease With Stanford Discovery Of Possible Cause

Date: 2006-11-29

A peacekeeper in the body's defenses against infection may hold the key to understanding - and eventually treating - Alzheimer's disease. Researchers at the Stanford University School of Medicine discovered that when a molecule responsible for dialing down the immune system malfunctions in the brain cells of mice, the rodents develop symptoms of the degenerative brain disease.

The finding, published in the November issue of the Journal of Clinical Investigation, offers researchers an insight into how humans may develop Alzheimer's, said the study's senior author Tony Wyss-Coray, PhD, associate professor of neurology and a researcher at the Veterans Affairs Palo Alto Health Care System.

Alzheimer's disease is characterized by an excessive buildup of proteins into plaques and tangles of cellular gunk that are likely to cause brain cells to die and lose their connections to other neurons. But for the most part, scientists do not understand the underlying biological problems behind Alzheimer's, making it difficult for doctors to treat, let alone cure.

"We don't have a treatment that alters the course of the disease," said Wyss-Coray.

Wyss-Coray and Ina Tesseur, PhD, an instructor in the Department of Neurology, examined thin slices of the brains of Alzheimer's patients who had died, and discovered abnormally low levels of a molecule involved in controlling the body's response to infection. That molecule allows the brain to detect and respond to TGF-beta, or transforming growth factor, a protein teeming through our bodies, involved in fighting infection, stopping cancer and perhaps keeping brain cells alive.

No other researchers had seen this change before, so Tesseur and Wyss-Coray set out to investigate whether it had some connection to Alzheimer's disease. They hypothesized that by protecting neurons, TGF-beta may help prevent Alzheimer's disease. If the TGF-beta pathway is turned off, the brain becomes more susceptible to a toxic buildup of proteins.

 

 

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© 2006 D M Kayed, MD, FAAN Dubai Neurology
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