Antibody against C-terminal Abeta selectively elevates plasma Abeta

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Abstract

Accumulation of amyloid β in the brain is a pathological hallmark of Alzheimer's disease, and the reduction of amyloid β has been proposed as a primary therapeutic target. Mice immunized against amyloid β and mice infused with anti-amyloid β antibody (active and passive immunization, respectively) have reduced brain amyloid β levels, and two mechanisms have been proposed: microglial phagocytosis in the brain and enhancement of amyloid β 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 β 40-specific antibody induces amyloid β sequestration. These results indicate that C-terminal antibodies may be useful in amyloid β sequestration therapy.

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