Microglia and inflammatory mechanisms in the clearance of amyloid beta peptide

Glia. 2002 Nov;40(2):260-269. doi: 10.1002/glia.10153.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Alzheimer Disease / complications
  • Alzheimer Disease / pathology
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / immunology
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Antigen-Antibody Complex / immunology
  • Antigen-Antibody Complex / metabolism
  • Antigens / immunology
  • Antigens / metabolism
  • Chemotaxis / immunology
  • Encephalitis / complications
  • Encephalitis / pathology
  • Encephalitis / physiopathology*
  • Humans
  • Microglia / immunology*
  • Microglia / metabolism*
  • Microglia / pathology
  • Phagocytosis / immunology

Substances

  • Amyloid beta-Peptides
  • Antigen-Antibody Complex
  • Antigens