Oct. 26, 2004 Alzheimer's disease is characterized by progressive loss of cognitive function due to amyloid-beta (Aß) deposits in the central nervous system. If these deposits could be stopped or slowed, Alzheimer's disease might become more manageable. In the current issue of the Journal of Alzheimer's Disease, a novel paper from researchers from the National Institute for Longevity Sciences, NCGG, Japan and Center for Neurological Diseases, Brigham & Women's Hospital, Harvard Institute of Medicine shows that a new oral vaccine treatment is effective in reducing Alzheimer's disease pathology.
Immunization results from the production of antibodies which attack the harmful agent, using the body's own defenses to remove the threat. In an earlier immunization study, 6 percent of the subjects developed acute meningoencephalitis, most likely caused by autoimmune T-cell activation. This caused the trial to be stopped. By developing vaccines that can minimize this T-cell activation while retaining the production of Aß-antibodies, a safer treatment might result.
The researchers attached Aß DNA to an adeno-associated virus vector and administered this vaccine to mice orally. Not only were the Aß levels decreased, but the T-cell immune response was significantly reduced. A single dose of this vaccine enhanced the production of Aß-antibodies for more than 6 months. Immunohistochemistry of the mouse brain tissue showed that the extra-cellular amyloid deposits were clearly decreased compared to the non-treated mouse.
Hideo Hara, M.D, writes "This new oral vaccine does not induce strong T cell immune reactions, and hence it could reduce the side effect of such meningoencephalitis…This new therapy seems to be effective for prevention and treatment of Alzheimer's disease."
The article is "Development of a safe oral Aß vaccine using recombinant adeno-associated virus vector for Alzheimer's disease" by Hideo Hara, Alon Monsonego, Katsutoshi Yuasa, Kayo Adachi, Xiao Xiao, Shin'ichi Takeda, Keikichi Takahashi, Howard L. Weiner and Takeshi Tabira. It appears in the Journal of Alzheimer's Disease, Vol.6, Number 5, published by IOS Press.
About the Journal of Alzheimer's Disease
The Journal of Alzheimer's Disease (http://www.j-alz.com) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer's disease. The journal publishes research reports, reviews, short communications, book reviews, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer's disease.
About IOS Press
Commencing its publishing activities in 1987, IOS Press (http://www.iospress.com) is a rapidly expanding scientific, technical, medical and professional publishing house focusing on a broad range of subject areas. Headquartered in Amsterdam, IOS Press publishes approximately 100 new books per annum and 60 international journals, covering topics ranging from computer science and mathematics to medicine and the natural sciences. Electronic access to all journals is now available. IOS Press also maintains offices in the Washington, DC area and Berlin and a co-publishing relationship with Ohmsha, Ltd (Tokyo).
Other social bookmarking and sharing tools:
The above story is based on materials provided by Case Western Reserve University.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Note: If no author is given, the source is cited instead.