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BioMed Research International
Volume 2014, Article ID 437483, 7 pages
Review Article

Microglia in Alzheimer’s Disease

1Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No. 5 Donghai Middle Road, Qingdao 266071, China
2Department of Pathology, Qingdao Municipal Hospital, Qingdao 266071, China
3Department of Neurology, Qingdao Municipal Hospital, College of Medicine and Pharmaceutics, Ocean University of China, Qingdao 266003, China
4Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing 210029, China

Received 26 February 2014; Revised 28 May 2014; Accepted 3 June 2014; Published 14 August 2014

Academic Editor: Jin-Tai Yu

Copyright © 2014 Ying Li et al. 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.


Alzheimer’s disease (AD) is a familiar neurodegenerative disease in the elderly. In this paper, we will review current viewpoints of microglial activation, inflammatory regulatory systems, and their relationship with AD pathology and etiology. Microglia cells are macrophage and representative of the innate immune system in brain. AD brain is marked by obvious inflammatory features, in which microglial activation is the driving force. β-amyloid protein sedimentation activates microglia cells, which causes the inflammation in AD. Microglia cells have dual roles: they provoke the release of inflammatory factors and cytotoxins leading to neuronal injuries and death; on the other hand, they have the neuroprotective effects. Through this, we hope to illustrate that the anti-inflammatory defenses of neurons can be practiced in the future strategy for recuperating the balance between the levels of inflammatory mediators and immune regulators in AD.