Immune System Offers New Alzheimer's Target

A specific dysfunction may encourage the disease, study finds

FRIDAY, June 10, 2005 (HealthDay News) -- An immune system defect may encourage the accumulation of amyloid-beta waste products in the brains of some Alzheimer's patients, according to a new study.

This oversaturation of the brain with amyloid-beta protein could lead to the formation of amyloid plaques -- the definitive hallmark of Alzheimer's disease.

The finding could lead to new ways of diagnosing and treating Alzheimer's by identifying and correcting this defect in the innate immune system, say researchers at the University of California, Los Angeles.

This is the first study to find that the innate -- the more primitive part -- of the immune system may be a factor in the development of Alzheimer's, the team adds.

In their study, published in the June 10 Journal of Alzheimer's Disease, the researchers compared blood samples from healthy people with those of Alzheimer's patients. In healthy people, innate immune system cells called macrophages easily cleared amyloid-beta in a test tube. In contrast, Alzheimer's patients' macrophages couldn't adequately perform this task.

"Macrophages are the janitors of the innate immune system, gobbling up waste products in the brain and throughout the body," study first author Dr. Milan Fiala said in a prepared statement.

The Alzheimer's patients' macrophages may not effectively bind to amyloid-beta or may have trouble in the absorption or uptake of amyloid-beta, Fiala said. This defect in the innate immune system may also be present in other conditions such as cardiovascular disease, which also involves a steady buildup of waste and plaque.

"If further study shows that this defective macrophage function is present in most Alzheimer's disease patients, new hormonal or immune-boosting approaches may offer new approaches to treating the disease," Fiala said.

More information

The U.S. National Institute on Aging has more about Alzheimer's disease.

SOURCE: University of California, Los Angeles, news release, June 10, 2005
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