Agents that alter blood levels of beta-amyloid protein in mouse models of Alzheimers disease represent a potential approach to treating the illness in humans that may be safer than the vaccine method of therapy, researchers report in a new study.
Beta-amyloid protein is a component of the amyloid plaques that accumulate in the brains of people with Alzheimer¡s disease. Beta-amyloid is viewed by many researchers and clinicians as the underlying cause of the degeneration and dementia that characterize the illness. Alzheimers disease is a progressive, degenerative brain disease and the most common form of dementia. There is no cure. Approximately four million Americans have the disease and some 14 million are expected to have it by 2050 unless a cure or preventive treatment is found.
"Recent evidence suggests that this protein in the peripheral circulation outside the brain may contribute to its accumulation in the brain," says study co-author Karen Duff, PhD, of the Center for Dementia Research, Nathan Kline Institute/New York University. The study, funded by the National Institutes of Health and the Alzheimers Association, appears in the January 1 issue of The Journal of Neuroscience.
Phil Kibak | EurekAlert!
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