Translocator protein 18 kDa (TSPO): old dogma, new mice, new structure, and new questions for neuroprotection
Many familial neurodegenerative genes whose mutations cause neuronal toxicity also enhance pro-inflammatory responses in microglia. [...]hyper-activation of the immune cells in the nervous system, termed "neuroinflammation", may not be the initiator of the neuropathologies, but rather may...
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Veröffentlicht in: | Neural regeneration research 2015-06, Vol.10 (6), p.878-880 |
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Sprache: | eng |
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Zusammenfassung: | Many familial neurodegenerative genes whose mutations cause neuronal toxicity also enhance pro-inflammatory responses in microglia. [...]hyper-activation of the immune cells in the nervous system, termed "neuroinflammation", may not be the initiator of the neuropathologies, but rather may be considered as one of the major contributors to disease progression, intimately implicated in a variety of neuronal diseases. In addition to the characteristic and dynamic morphological changes, inflammatory activation of microglia induces a change in their gene expression profiles. [...]immunological detection of marker proteins, such as IBA-1 or CD11b, has been commonly used to monitor microglia activation in the nervous system. [...]the traditionally used immunohistochemical techniques have limitations and are not easily applicable to in vivo situations. [...]there is an imminent need for the development of biological markers and probes to monitor neuroinflammation in vivo. [...]the new name TSPO was suggested to more accurately represent the key molecular function of this molecule regardless of its subcellular or tissue distribution. [...]the ubiquitous expression and evolutionary conservation of TSPO from bacteria to mammals strongly suggested its essential role in cellular processes. |
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ISSN: | 1673-5374 1876-7958 |
DOI: | 10.4103/1673-5374.158338 |