Antibody Stops Alzheimer's in Mice

May Lead to New Treatments to Protect Human Brains

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Oct. 30, 2002 -- Scientists have come up with a new and potentially more promising way to stop Alzheimer's disease in its tracks, at least in mice. A new study shows that an antibody can both block the production of the brain-clogging amyloid plaques found in Alzheimer's as well as move existing plaques out of the brain and into the bloodstream.

It's the third method reported for halting the development of the memory-robbing disease in mice. But researchers say this approach is especially promising because it uses antibodies that are already being studied extensively in clinical trials for the treatment of other diseases.

The other two techniques use vaccination or anti-inflammatory drugs to treat the disease and reduce plaque formation.

This new method, described in a study published in today's online issue of Nature Neuroscience, uses an antibody that blocks a protein, known as the CD40-CD40L protein, that seems to play a vital role in depositing the amyloid plaques in the brain. The study shows that injecting the antibody in mice that are genetically engineered to develop Alzheimer's results in a 60% reduction in plaque formation.

In addition, researchers also found that some of the plaques that had already formed were moved out of the brain and into bloodstream in mice that received the injection.

The study authors say the results suggest that blocking the CD40-CD40L protein in either people at risk for Alzheimer's or those in the early stages of the disease would prevent any further accumulation of the plaques in the brain and, therefore, would prevent the disease from progressing.

"The use of antibodies to the CD40 system has not be previously associated with Alzheimer's amyloid deposition, although the antibodies are currently in clinical trials to treat other diseases," says study author Michael Mullan, MD, PhD, director of the Roskamp Institute in Tampa, Fla., in a news release.

He says these findings are significant because they place not just inflammation but the entire immune response as central to the development of Alzheimer's.

Researchers say these results will help scientists understand what causes Alzheimer's disease as well as potentially lead to new treatments.

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