Microglia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Microglia are a type of glial cell that act as the immune cells of the Central nervous system (CNS). Microglia, the smallest of the glial cells, can act as phagocytes, cleaning up CNS debris. Most serve as representatives of the immune system in the brain and spinal cord.

Microglia are close cousins of other phagocytic cells including macrophages and dendritic cells.

Microglia are thought to be highly mobile cells that play numerous important roles in protecting the nervous system.

Origin

Microglia are derived from myeloid progenitor cells (as are macrophages and dendritic cells) which come from the bone marrow. During embryonic development, however, they migrate to the CNS to differentiate into microglia.

Further development

After phagocytosis of lipid droplets and other debris (usually from tissue necrosis), microglia are termed gitter cells. A gitter cell is globular and swollen and can also be called a compound granule cell or compound granular corpuscle.

Clinical significance

Microglia are also thought to play a role in neurodegenerative disorders such as Alzheimer’s disease, dementia, multiple sclerosis and Amyotrophic lateral sclerosis. They are responsible for producing an inflammatory reaction to brain trauma ^[1] and are the main HIV-1 target cells in the central nervous system.^[2].

History

Babes described activation of microglia in a rabies case in 1897, but did not know what the clusters of microglia he saw were (Streit et al., 2004). Franz Nissl and F. Robertson first described microglial cells, and Pio del Rio-Hortega, a student of Santiago Ramón y Cajal, first called the cells “microglia” around 1920 [2]. Cell staining techniques in the 1980s showed that microglia are related to macrophages.

References

↑ There is some debate in the scientific community as to the effects of microglia; while microglia have been proven to exhibit neuroprotective effects (i.e. inducing neuronal banching), they have also been found responsible for much of the secondary neuronal damage through the secretion of reactive oxygen species. On the other side they have a positive effect in Alzheimer’s disease by degrading the so-called [amyloid] plaques. Streit WJ, Mrak RE, Griffin WS. (2004). “Microglia and neuroinflammation: a pathological perspective”. J Neuroinflammation. 1 (1): 14. PMID 15285801.
↑ Marban C, Suzanne S, Dequiedt F, de Walque S, Redel L, Van Lint C, Aunis D, Rohr O. (2007). “Recruitment of chromatin-modifying enzymes by CTIP2 promotes HIV-1 transcriptional silencing”. The EMBO journal. 26 (2): 412–423. PMID 17245431.

External links

Microglia home page at microglia.net
The Role of Microglia in the Central Nervous System – Clinical Microbiolgy Reviews October 2004, p. 942-964, Vol. 17, No. 4
Creeping into your Head – A Brief Introduction to Microglia – A Review from the Science Creative Quarterly
“Immune Scavengers Target Alzheimer’s Plaques”. Retrieved 2007-05-09. Text ” NEUROSCIENCE: Immune Scavengers Target Alzheimer’s Plaques ” ignored (help); Text ” April 6, 2007 ” ignored (help) – from Harvard University

Template:Blood

fa:میکروگلیال he:מיקרוגליה

Template:WikiDoc Sources

[Streit-1] There is some debate in the scientific community as to the effects of microglia; while microglia have been proven to exhibit neuroprotective effects (i.e. inducing neuronal banching), they have also been found responsible for much of the secondary neuronal damage through the secretion of reactive oxygen species. On the other side they have a positive effect in Alzheimer’s disease by degrading the so-called [amyloid] plaques. Streit WJ, Mrak RE, Griffin WS. (2004). “Microglia and neuroinflammation: a pathological perspective”. J Neuroinflammation. 1 (1): 14. PMID 15285801.

[Marban-2] Marban C, Suzanne S, Dequiedt F, de Walque S, Redel L, Van Lint C, Aunis D, Rohr O. (2007). “Recruitment of chromatin-modifying enzymes by CTIP2 promotes HIV-1 transcriptional silencing”. The EMBO journal. 26 (2): 412–423. PMID 17245431.

[1]

[2]