Based on these results, the researcher now believes that removing plaques -- at least by this method -- is unlikely to make a significant difference to the clinical outcome of patients with established Alzheimer's disease. "In addition, it strongly suggests that plaques are not sufficient on their own to account for disease progression," Holmes said.
Based on the findings, novel strategies for the treatment of Alzheimer's disease should not focus on the removal of plaques in patients with established Alzheimer's, Holmes contends. "Treatments should move towards preventing plaques from building up in the first place," he said. "Or in established Alzheimer's disease, treatments should focus more on non-plaque therapies."
Dr. Sam Gandy, chairman of the Alzheimer's Association's National Medical and Scientific Advisory Council, said the new finding suggests that other forces besides plaque build-up are driving disease progression.
"If you don't start with your vaccine until you are at a later stage of disease and other processes are already established, the horse may be already out of the barn," Gandy said. "It is possible that amyloid is like a match lighting a fire and once the fire is out of control, dealing with the match isn't that effective."
But there was better news in a second study. In that work, Dr. Rachelle S. Doody, a professor of neurology at the Alzheimer's Disease and Memory Disorders Center at Baylor College of Medicine in Houston, and her colleagues studied the effects of the drug dimebon on 183 patients in Russia with mild to moderate Alzheimer's disease. The drug is currently not marketed anywhere, and was previously used in Russia as an antihistamine.
"This is a medication that has not previously been studied in Alzheimer's disease," Doody said. In the trial, patients were randomly assigned to 20 milligrams of dimebon th
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