Abstract

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. © 2002 Wiley‐Liss, Inc.

Keywords

MicrogliaPhagocytosisPhagocyteAmyloid (mycology)NeuroscienceBiologyPeptideNeuroinflammationAlzheimer's diseaseTREM2Biochemistry of Alzheimer's diseaseAmyloid betaMononuclear phagocyte systemImmunologyInflammationComplement systemReceptorAmyloid precursor proteinDiseaseImmune systemBiochemistryPathologyMedicine

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Year
2002
Type
review
Volume
40
Issue
2
Pages
260-269
Citations
374
Access
Closed

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Joseph Rogers, Ron Strohmeyer, Carl J. Kovelowski et al. (2002). Microglia and inflammatory mechanisms in the clearance of amyloid β peptide. Glia , 40 (2) , 260-269. https://doi.org/10.1002/glia.10153

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DOI
10.1002/glia.10153