Abeta N-terminal-end specific antibody reduced beta-amyloid in Alzheimer-model mice.

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease with memory dysfunction that is causing serious medical problems in modern society. For the fundamental treatment of AD, an amyloid beta protein (Abeta) vaccine is considered to be the most potent candidate. To cure AD, we developed Abeta N-terminal-end specific monoclonal antibody named 82E1, which does not cross-react with full-length Abeta precursor. Passive intraperitoneal administration of 82E1 markedly reduced total plaque area (Abeta burden) in the Tg2576 mouse brains. This was confirmed by the ELISA measurement of insoluble Abeta in the brain homogenates. The density of diffuse plaques, which increases in the late stage, was markedly reduced by the administration of 82E1, suggesting that the reduction of the Abeta burden was due to the prevention of newly developed diffuse plaques. Above results provide an insight into the further therapeutic intervention in AD with few adverse effects.