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Gene Studies Could Point to New Alzheimer's Treatments
Date:4/25/2013

33 in microglia was linked to higher levels of the beta-amyloid protein plaques that have long been associated with Alzheimer's disease.

In their experiments with mice, switching off CD33 activity seemed to help microglia sweep away the plaques.

"Our findings suggest that pharmaceutical inactivation of CD33 represents a potentially powerful new therapy for the treatment and prevention of Alzheimer's disease, and perhaps other neurodegenerative disorders," senior study author Rudolph Tanzi, of Massachusetts General Hospital and Harvard Medical School in Boston, said in a journal news release.

Another expert said the findings from both studies may help advance research.

"We have known for a long time that Alzheimer's disease is characterized by the presence of excessive inflammation in the brain," said Philippe Marambaud, an investigator at the Litwin-Zucker Research Center for the Study of Alzheimer's Disease at the Feinstein Institute for Medical Research in Manhasset, N.Y.

"The role of this inflammatory response in the pathogenic mechanisms of the disease, however, remains unclear," he said. "These two studies ... provide concordant evidence that the immune cells microglia actively participate in this disease process."

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about Alzheimer's disease.

-- Robert Preidt

SOURCES: Philippe Marambaud, Ph.D., investigator, Litwin-Zucker Research Center for the Study of Alzheimer's Disease, Feinstein Institute for Medical Research, Manhasset, N.Y.; Cell, news release, April 25, 2013; Neuron,news release, April 25, 2013; Icahn School of Medicine at Mount Sinai, New York City, news release, April 25, 2013


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