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International Journal of Inflammation
Volume 2017 (2017), Article ID 8385961, 20 pages
Review Article

Sterile Neuroinflammation and Strategies for Therapeutic Intervention

1Cerebrovascular Research, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA
2Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA
3Department of Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA

Correspondence should be addressed to Manoj Banjara and Chaitali Ghosh

Received 16 September 2016; Accepted 13 December 2016; Published 3 January 2017

Academic Editor: David A. Hart

Copyright © 2017 Manoj Banjara and Chaitali Ghosh. 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.


Sterile neuroinflammation is essential for the proper brain development and tissue repair. However, uncontrolled neuroinflammation plays a major role in the pathogenesis of various disease processes. The endogenous intracellular molecules so called damage-associated molecular patterns or alarmins or damage signals that are released by activated or necrotic cells are thought to play a crucial role in initiating an immune response. Sterile inflammatory response that occurs in Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, hemorrhage, epilepsy, or traumatic brain injury (TBI) creates a vicious cycle of unrestrained inflammation, driving progressive neurodegeneration. Neuroinflammation is a key mechanism in the progression (e.g., AD and PD) or secondary injury development (e.g., stroke, hemorrhage, stress, and TBI) of multiple brain conditions. Hence, it provides an opportunity for the therapeutic intervention to prevent progressive tissue damage and loss of function. The key for developing anti-neuroinflammatory treatment is to minimize the detrimental and neurotoxic effects of inflammation while promoting the beneficial and neurotropic effects, thereby creating ideal conditions for regeneration and repair. This review outlines how inflammation is involved in the pathogenesis of major nonpathogenic neuroinflammatory conditions and discusses the complex response of glial cells to damage signals. In addition, emerging experimental anti-neuroinflammatory drug treatment strategies are discussed.