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Title: Antibody against C-terminal Abeta selectively elevates plasma Abeta. Author: Gray AJ, Sakaguchi G, Shiratori C, Becker AG, LaFrancois J, Aisen PS, Duff K, Matsuoka Y. Journal: Neuroreport; 2007 Feb 12; 18(3):293-6. PubMed ID: 17314674. Abstract: Accumulation of amyloid beta in the brain is a pathological hallmark of Alzheimer's disease, and the reduction of amyloid beta has been proposed as a primary therapeutic target. Mice immunized against amyloid beta and mice infused with anti-amyloid beta antibody (active and passive immunization, respectively) have reduced brain amyloid beta levels, and two mechanisms have been proposed: microglial phagocytosis in the brain and enhancement of amyloid beta efflux by antibodies present in the periphery (sequestration). The optimal antibody for microglial phagocytosis has been shown to be N-terminal-specific antibody; however, the potency of C-terminal-specific antibody in sequestration remains unclear. In this study, we found that anti-amyloid beta 40-specific antibody induces amyloid beta sequestration. These results indicate that C-terminal antibodies may be useful in amyloid beta sequestration therapy.[Abstract] [Full Text] [Related] [New Search]