Glia. 2002 Nov;40(2):260-9.

Microglia and inflammatory mechanisms in the clearance of amyloid beta peptide.

Rogers J, Strohmeyer R, Kovelowski CJ, Li R.

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Sun Health Research Institute, Sun City, Arisona 85372, USA. jrogers@mail.sunhealth.org

Abstract

There is now abundant evidence that brain microglia, when activated, have the lineage, receptors, and synthetic capacity to participate in both potentially neurotoxic inflammatory responses and potentially beneficial phagocytic responses. Amyloid beta peptide (Abeta) forms highly insoluble, beta-pleated aggregates that are widely deposited in the Alzheimer's disease (AD) cortex and limbic system. Aggregated Abeta also activates the classical and alternative complement cascades. These properties make Abeta an excellent target for microglial phagocytosis, a view supported by multiple reports, through well established mechanisms of phagocyte clearance.

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