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International Journal of Alzheimer’s Disease
Volume 2012, Article ID 737846, 9 pages
Review Article

The Biphasic Role of Microglia in Alzheimer's Disease

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan

Received 28 December 2011; Accepted 29 February 2012

Academic Editor: Akio Suzumura

Copyright © 2012 Tetsuya Mizuno. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Neuroinflammation is involved in the pathogenesis of Alzheimer's disease (AD). Microglia, macrophage-like resident immune cells in the brain, play critical roles in the inflammatory aspects of AD. Microglia may be activated by oligomeric and fibrillar species of amyloid β (Aβ) that are constituents of senile plaques and by molecules derived from degenerated neurons, such as purines and chemokines, which enhance their migration and phagocytosis. The main neurotoxic molecules produced by activated microglia may be reactive oxygen species, glutamate, and inflammatory cytokines such as tumor-necrosis-factor-α and interleukin- (IL-) 1β These molecules differentially induce neurotoxicity. Aβ itself directly damages neurons. In terms of neuroprotective properties, microglia treated with fractalkine or IL-34 attenuate Aβ neurotoxicity by Aβ clearance and the production of antioxidants. Therefore, regulation of the microglial role in neuroprotection may be a useful therapeutic strategy for AD.