Microglia and inflammatory mechanisms in the clearance of amyloid β peptide

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 β peptide (Aβ) forms highly insoluble, β‐pleated aggregates that are widely deposited in the Alzheimer's disease (AD) cortex and limbic system. Aggregated Aβ also activates the classical and alternative complement cascades. These properties make Aβ an excellent target for microglial phagocytosis, a view supported by multiple reports, through well established mechanisms of phagocyte clearance. GLIA 40:260–269, 2002.