Document Detail


Microglial activation and its implications in the brain diseases.
MedLine Citation:
PMID:  17504139     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
An inflammatory process in the central nervous system (CNS) is believed to play an important role in the pathway leading to neuronal cell death in a number of neurodegenerative diseases including Parkinson's disease, Alzheimer's disease, prion diseases, multiple sclerosis and HIV-dementia. The inflammatory response is mediated by the activated microglia, the resident immune cells of the CNS, which normally respond to neuronal damage and remove the damaged cells by phagocytosis. Activation of microglia is a hallmark of brain pathology. However, it remains controversial whether microglial cells have beneficial or detrimental functions in various neuropathological conditions. The chronic activation of microglia may in turn cause neuronal damage through the release of potentially cytotoxic molecules such as proinflammatory cytokines, reactive oxygen intermediates, proteinases and complement proteins. Therefore, suppression of microglia-mediated inflammation has been considered as an important strategy in neurodegenerative disease therapy. Several anti-inflammatory drugs of various chemical ingredients have been shown to repress the microglial activation and to exert neuroprotective effects in the CNS following different types of injuries. However, the molecular mechanisms by which these effects occur remain unclear. In recent years, several research groups including ours have attempted to explain the potential mechanisms and signaling pathways for the repressive effect of various drugs, on activation of microglial cells in CNS injury. We provide here a comprehensive review of recent findings of mechanisms and signaling pathways by which microglial cells are activated in CNS inflammatory diseases. This review article further summarizes the role of microglial cells in neurodegenerative diseases and various forms of potential therapeutic options to inhibit the microglial activation which amplifies the inflammation-related neuronal injury in neurodegenerative diseases.
Authors:
S Thameem Dheen; Charanjit Kaur; Eng-Ang Ling
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Current medicinal chemistry     Volume:  14     ISSN:  0929-8673     ISO Abbreviation:  Curr. Med. Chem.     Publication Date:  2007  
Date Detail:
Created Date:  2007-05-16     Completed Date:  2007-06-28     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9440157     Medline TA:  Curr Med Chem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1189-97     Citation Subset:  IM    
Affiliation:
Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Blk MD10, 4 Medical Drive, Singapore 117597.
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MeSH Terms
Descriptor/Qualifier:
Amyloid beta-Protein / physiology
Animals
Endocannabinoids / pharmacology
Glucocorticoids / pharmacology
Humans
Interferon-gamma / physiology
Lipopolysaccharides / pharmacology
Macrophage Colony-Stimulating Factor / physiology
Microglia / drug effects,  physiology*
Minocycline / pharmacology
Nerve Regeneration
Neurodegenerative Diseases / physiopathology*
Organogenesis
Prions / pharmacology
Proteochondroitin Sulfates / physiology
Signal Transduction
Thrombin / physiology
Transforming Growth Factor beta1 / physiology
Vitamins / pharmacology
Chemical
Reg. No./Substance:
0/Amyloid beta-Protein; 0/Endocannabinoids; 0/Glucocorticoids; 0/Lipopolysaccharides; 0/Prions; 0/Proteochondroitin Sulfates; 0/Transforming Growth Factor beta1; 0/Vitamins; 10118-90-8/Minocycline; 81627-83-0/Macrophage Colony-Stimulating Factor; 82115-62-6/Interferon-gamma; EC 3.4.21.5/Thrombin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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