Potential Vaccine for Alzheimer’s Disease Improves Learning and Memory Deficits in Mice
For immediate release.
NEWS RELEASE NR-05-06 (05/2/06). For more information, please contact Tracey Somers at (202) 962-4000 or tsomers@sfn.org.
POTENTIAL VACCINE FOR ALZHEIMER’S DISEASE IMPROVES LEARNING AND MEMORY DEFICITS IN MICE
WASHINGTON, DC, May 2, 2006 - A vaccine for Alzheimer's disease improves learning and memory deficits in mice, according to a new study.
"While there are several promising strategies for delaying or preventing Alzheimer's disease, this new vaccine might be able to treat the disease, giving the brain the best chance at recovery," says Samuel Gandy, MD, PhD, at the Farber Institute for Neurosciences of the Thomas Jefferson University and chair of the National Medical and Scientific Advisory Council of the Alzheimer's Association. This study appears in the May 3 issue of The Journal of Neuroscience.
"This is the first study to report combined immunological, neuropathological, and behavioral benefits of a new vaccine using a modified amyloid protein in an Alzheimer's disease mouse model," says senior author Cynthia Lemere, PhD, at the Brigham and Women's Hospital and Harvard Medical School. "Our findings show promise for a potentially safer and more effective Alzheimer's vaccine in humans," she adds.
One theory on Alzheimer's disease is that amyloid-beta plaques--clumps of protein that build up between nerve cells in the brain--contribute to cognitive and behavioral deficits. Scientists, including Lemere and first author Marcel Maier, developed a vaccine using a special type of amyloid-beta substance capable of triggering the body's immune system to produce antibodies--molecules that attack foreign invaders--which reduced the build up of amyloid-beta plaques in the brains of mice and led to improved learning and memory. The vaccine was administered via nose drops and targeted only the region of the amyloid-beta protein that is important for generating antibodies against amyloid-beta.
The targeted vaccine avoided the immune response in mice thought to be responsible for the dangerous side effect of brain inflammation that a previous Alzheimer's disease vaccine encountered in humans, and still produced antibodies successful in clearing brain amyloid deposits. Moreover, the vaccine was administered via the nose, which will likely be more tolerable to patients as a preventative strategy in the increasingly aging population.
"Next, we plan to further refine our novel vaccine and prepare for possible human trials," says Lemere.
Alzheimer's affects an estimated 4.5 million Americans at a cost annually of at least $100 billion. Several medications are approved to treat the disorder, but none can stop the underlying degeneration of brain cells.
The Journal of Neuroscience is published by the Society for Neuroscience, an organization of more than 37,500 basic scientists and clinicians who study the brain and nervous system. Cynthia Lemere, PhD, can be reached at clemere@rics.bwh.harvard.edu.
