Background: Over the past few years, amyloid beta protein (Aβ) vaccination has become one of the most effective treatments for Alzheimer’s disease.However, the appearance of severe side effects during clinical trials has highlighted the need for improved safety and efficacy.Although antibodies directed against the amino (N)-termini of Aβ are highly effective for passive immunization, a substantial risk of inducing cerebral hemorrhage has been documented. Objective: We investigated the effect of the administration of BC05, which was the first antibody developed against the carboxyl (C)-termini of Aβ42(43), on the clearance of brain Aβ42(43). Method: The BC05 antibody was injected into the peritoneal cavity of Tg2576 transgenic mice expressing βAPPKM670/671NL once a week from 3 to 12 months of age. Results: BC05 caused a selective 44-fold increase in plasma Aβ42(43) and a significant increase in brain soluble Aβ42(43), showing a 156% difference. Brain insoluble Aβ40 and Aβ42(43) levels were decreased by 27.3 and 31.5%, respectively. A reduction in the number of BAN50-labeled plaques was observed. Conclusions: BC05 might render Aβ42(43) soluble within the brain and inhibit the insoluble deposition of Aβ40 and Aβ42(43). By analyzing the mechanism of the elevation of soluble Aβ42(43) after passive immunization of BC05, safer and more effective methods of immunotherapy for Alzheimer’s disease might be developed.

Keywords:
Alzheimer’s disease, Amyloid beta protein, Immunotherapy, Alzheimer’s disease, Passive immunization
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© 2005 S. Karger AG, Basel
2005
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