Microglia in Disease
Microglia and inflammatory mechanisms in the clearance of amyloid β peptide
Article first published online: 4 OCT 2002
Copyright © 2002 Wiley-Liss, Inc.
Special Issue: Microglia
Volume 40, Issue 2, pages 260–269, November 2002
How to Cite
Rogers, J., Strohmeyer, R., Kovelowski, C.J. and Li, R. (2002), Microglia and inflammatory mechanisms in the clearance of amyloid β peptide. Glia, 40: 260–269. doi: 10.1002/glia.10153
- Issue published online: 4 OCT 2002
- Article first published online: 4 OCT 2002
- Manuscript Accepted: 1 JUL 2002
- Manuscript Received: 14 FEB 2002
- National Institute on Aging. Grant Number: AGO7367
- Alzheimer's Association
- amyloid β peptide
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.