期刊
NEUROREPORT
卷 18, 期 3, 页码 293-296出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0b013e3280148e76
关键词
Alzheimer's disease; amyloid beta; antibody; C-terminus; immunization; passive immunization; sequestration; therapy
资金
- NIA NIH HHS [AG022455, AG027398] Funding Source: Medline
Accumulation of amyloid P 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 annyloid 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 annyloid beta sequestration. These results indicate that C-terminal antibodies may be useful in annyloid beta sequestration therapy.
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