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Protein Clumps May Appear Years Before Memory Problems
Date:7/29/2009

Discovery could help in Alzheimer's prevention efforts, researcher says,,

WEDNESDAY, July 29 (HealthDay News) -- Amyloid protein deposits in the brain play a role in disrupting the memory formation process long before a person shows symptoms of the memory impairment of Alzheimer's disease, a new study contends.

Previous research had suggested that clumps of amyloid protein, which damage neurons and are characteristic of Alzheimer's disease, begin appearing many years before Alzheimer's symptoms appear. But the link between the deposits and memory impairment had not been clearly demonstrated in humans.

In the new study, which appears in the July 30 issue of Neuron, U.S. researchers used medical imaging to examine the brains of older people who did not have significant memory impairment.

"Two recent advances in neuroimaging now allow us to explore the early, asymptomatic phase of [Alzheimer's disease], the ability to measure amyloid distribution in living humans and the identification of sensitive markers of brain dysfunction" in the disease, Dr. Reisa Sperling, of the Center for Alzheimer's Research and Treatment at Brigham and Women's Hospital in Boston and lead author of the study, said in a news release from the journal's publisher.

The researchers found that a number of study participants had amyloid deposits and abnormal activity in areas of the brain believed to be involved in memory function.

The results could help in efforts to find ways to predict and treat cognitive decline in people at risk for Alzheimer's, the study authors noted.

"Longitudinal studies are certainly needed, but our findings are consistent with the premise that cognitively intact older individuals with amyloid pathology may already be in the early stages of [Alzheimer's disease]," Sperling said. "The combination of molecular and functional imaging techniques may prove useful in monitoring disease progression prior to significant clinical symptoms, as well as the response to amyloid-modifying therapeutic agents in subjects at risk for developing [Alzheimer's disease]."

More information

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



-- Robert Preidt



SOURCE: Cell Press, news release, July 29, 2009


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