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WEDNESDAY, July 30 (HealthDay News) — New reports on very different approaches to treating Alzheimer's disease could one day lead to better therapies for the mind-robbing condition, experts say.
A trio of studies that were presented Wednesday at the Alzheimer's Association 2008 International Conference on Alzheimer's Disease in Chicago noted progress made on three different treatment fronts.
The first involves a drug called Dimebon, with positive results being reported from tests in Russia. Dimebon is an antihistamine, and data from the Russian trials indicated that Dimebon might have value in treating Alzheimer's.
This buttressed American research reported earlier this year that showed improvements in Alzheimer's patients given Dimebon in a controlled study. The drug is believed to prevent the death of brain cells.
Researchers at the University of California, Los Angeles, studied 183 people who had mild to moderate Alzheimer's disease. Mental function remained stable in those taking the drug, while it declined in those given a placebo. Mental function also stabilized in people who were first given a placebo after they began taking Dimebon.
Another trial used the body's immune system to prevent the mental deterioration suffered by people with Alzheimer's disease. The immune attack is aimed at the deposits of beta-amyloid protein that accumulate in the brains of patients.
"The idea has been around for almost a decade now," Nixon. "The initial notion was to use the vaccine approach to prevent amyloid deposition, injecting amyloid so the body would attack the deposits. Now we are into phase two, injecting the antibody itself."
Researchers at Eli Lilly & Co. reported on 52 people with mild to moderate Alzheimer's. Some were given weekly injections of a monoclonal antibody that binds to beta amyloid, while others were injected with a placebo.
Detailed measurements showed an increased level of beta amyloid in both blood and cerebrospinal fluid after 12 weeks in those getting the antibody, an indication that the beta amyloid in the brain might be starting to dissolve, the researchers said. New studies of the therapy are planned.
Nixon viewed the results with "tempered optimism." One interesting finding was the response to the therapy was greatest in people who did not have a known genetic marker for Alzheimer's risk, he said. "What is the significance of this? Why do carriers not respond?" Nixon asked. The answer might help explain Alzheimer's disease better, he said.
A third study using a broad spectrum of antibodies was reported by a team at Weill Cornell Medical College in New York City. The treatment, originally developed by Baxter International to treat autoimmune conditions, was given to 24 people with mild to moderate Alzheimer's disease in a set of trials extending as long as 18 months. Statistically significant increases in mental function were seen in those getting the treatment, the researchers said. A large-scale, 18-month follow-up trial will be done.
SOURCES: Ralph Nixon, M.D., professor, psychiatry and cell biology, New York University; July 30, 2008, presentations, Alzheimer's Association 2008 International Conference on Alzheimer's Disease, Chicago
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