David M. Holtzman, M.D., the Paul and Charlotte Hagemann Professor of Neurology and professor of molecular biology and pharmacology, has received two awards for his Alzheimer’s disease research: the 2003 Potamkin Prize for Research in Picks, Alzheimer’s Disease and Related Disorders; and the Promising Work Award from MetLife Foundation.
“These are two of the most prestigious prizes in Alzheimer’s research,” said John C. Morris, M.D., co-director of the Alzheimer’s Disease Research Center and the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology. “Dave’s work already has dramatically improved our understanding of how brain plaques develop in individuals with Alzheimer’s disease and has the potential to lead to better diagnostic methods and perhaps even a cure.”
The Potamkin prize will be awarded April 2 at the 2003 American Academy of Neurology annual meeting at the Hawaii Convention Center in Honolulu. The MetLife award was recently presented at the Awards for Medical Research event in Washington, D.C.
As part of the Potamkin prize, Holtzman will share a $100,000 award with the other prize recipient, Ashley Bush, M.D., of Massachusetts General Hospital. He also received a $100,000 institutional grant as part of the MetLife award to further his research.
Holtzman’s laboratory specializes in studying the early, silent stages of Alzheimer’s disease. His team played a leading role in showing how dangerous amounts of a protein called amyloid-beta (ABeta) begin to accumulate in the brain many years before symptoms arise. Work from the Holtzman lab has shown that two proteins, apolipoprotein E (apoE) and apolipoprotein J (apoJ) play an important role in the buildup and toxicity of ABeta in the brain.
In collaboration with scientists at Eli Lilly and Co., Holtzman’s team identified a monoclonal antibody called m266, which, in mice, draws ABeta out of the brain and into the blood. In a March 2002 issue of the journal Science, the team published the successful use of m266 to identify Alzheimer’s-type changes in living mice. The test is one of the first proposed blood tests to diagnose the disease before clinical symptoms arise.
Since m266 appears to result in clearing of ABeta out of the brain, it may also assist in breaking down amyloid plaques and thereby help treat the disease. Several companies now are considering clinical trials to determine whether administration of anti-ABeta antibodies improves cognitive symptoms in individuals with Alzheimer’s disease.
“Tremendous advances have been made in our understanding of Alzheimer’s disease over the last 15 years by scientists around the world,” Holtzman said. “We are hopeful that in a relatively short time, some of these advances will translate into much more effective strategies for diagnosing, preventing and treating this disease.”