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Neuroprotective function in brain microglia
- Source :
- Current Anaesthesia & Critical Care. 20:142-147
- Publication Year :
- 2009
- Publisher :
- Elsevier BV, 2009.
-
Abstract
- Summary Microglia are uniformly distributed throughout the central nervous system. The number of microglia is thought to make up 5–20% of the entire glial cell population. Origin of microglia has been discussed for several decades. Recently, microglia are widely considered to originate from mesodermal monocyte/macrophage cell lineage, because of similarities in cell surface molecular phenotype. In normal adult brain, microglia have finely branched and ramified cell processes that extend in all directions, and survey the brain microenvironment. When the brain is injured by trauma, stroke and other neurodegenerative disorders, microglia transform their morphology into an activated phenotype, and accumulate in the affected sites. Activation of microglia has been believed to lead to neurotoxic effect, because of results of the in vitro culture studies, which reflects only one possible phenotype of microglia. However, recent studies in the in vivo brain revealed that microglia play a crucial role in neuroprotection against neural cell injury such as cerebral ischemia. Thus, microglial function under pathological conditions in the CNS remains a controversial subject, because of their complexity. In the present review, we summarized the current findings of microglial function, and discussed the possibility of the application to a novel therapeutic strategy.
- Subjects :
- education.field_of_study
Microglia
Neurodegeneration
Population
Central nervous system
Biology
Critical Care and Intensive Care Medicine
medicine.disease
Neuroprotection
Phenotype
Transplantation
Anesthesiology and Pain Medicine
medicine.anatomical_structure
nervous system
medicine
education
Neuroscience
Neuroinflammation
Subjects
Details
- ISSN :
- 09537112
- Volume :
- 20
- Database :
- OpenAIRE
- Journal :
- Current Anaesthesia & Critical Care
- Accession number :
- edsair.doi...........d3f507e2541a5fbee815930a63f61ea6
- Full Text :
- https://doi.org/10.1016/j.cacc.2008.12.007