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Brain Advance Access published online on June 20, 2008
Brain, doi:10.1093/brain/awn109
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© 2008 The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Review Article

Debris clearance by microglia: an essential link between degeneration and regeneration

H. Neumann1, M. R. Kotter2,3 and R. J. M. Franklin4

1Neural Regeneration, Institute of Reconstructive Neurobiology, University Bonn, Bonn, Germany, 2Department of Neurosurgery, Medical University Vienna, Vienna, Austria, 3Department of Neurosurgery, University of Göttingen, Göttingen, Germany and 4Department of Veterinary Medicine and Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK

Correspondence to: Harald Neumann, Neural Regeneration, Institute of Reconstructive Neurobiology, University Bonn and Hertie-Foundation, Sigmund-Freud-Str. 25, 53127 Bonn, Germany E-mail: hneuman1{at}uni-bonn.de

Microglia are cells of myeloid origin that populate the CNS during early development and form the brain's innate immune cell type. They perform homoeostatic activity in the normal CNS, a function associated with high motility of their ramified processes and their constant phagocytic clearance of cell debris. This debris clearance role is amplified in CNS injury, where there is frank loss of tissue and recruitment of microglia to the injured area. Recent evidence suggests that this phagocytic clearance following injury is more than simply tidying up, but instead plays a fundamental role in facilitating the reorganization of neuronal circuits and triggering repair. Insufficient clearance by microglia, prevalent in several neurodegenerative diseases and declining with ageing, is associated with an inadequate regenerative response. Thus, understanding the mechanism and functional significance of microglial-mediated clearance of tissue debris following injury may open up exciting new therapeutic avenues.

Key Words: neuroinflammation; microglia; neurodegeneration; regeneration; phagocytosis; multiple sclerosis, Alzheimer disease

Abbreviations: Aβ, amyloid-β; BDNF, brain derived neurotrophic factor; CR3, complement receptor type 3; EAE, experimental autoimmune encephalomyelitis; IGF-1, insulin-like growth factor-1; IL-4, interleukin-4; TLRs, toll like receptors; TNF-{alpha}, tumour necrosis factor-{alpha}; TREM-2, triggering receptor expressed on myeloid cells-2

Received March 5, 2008. Revised May 8, 2008. Accepted May 9, 2008.


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