Source:http://linkedlifedata.com/resource/pubmed/id/20504160
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2010-8-17
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pubmed:abstractText |
Traumatic brain injury (TBI) is one of the most acute degenerative pathologies in the central nervous system, and in vivo indices enabling an assessment of TBI on a mechanistic basis have yet to be established. The aim of this work was to pursue neuroinflammatory changes and their link to functional disruptions of traumatically-damaged neurons in a rat model of TBI by longitudinal positron emission tomographic (PET) assays. TBI was induced in the unilateral frontal cortex of craniotomied rats according to a lateral fluid percussion brain injury protocol. The use of [(18)F]fluoroethyl-DAA1106 as a PET tracer for translocator protein (TSPO) permitted demonstration of the inflammatory response to the injury, peaking at 1 week after impact. This alteration was parallel to metabolic deficits assessed by PET with [(18)F]fluorodeoxyglucose, but the difference in TSPO levels between impacted and non-impacted frontal cortices was more than threefold of the interlateral metabolic difference, indicating superiority of TSPO imaging for sensitive detection of post-traumatic pathologies. Comparative PET, autoradiographic. and immunohistochemical investigations illustrated the primary contribution of hypertrophic microglia and macrophages to acute TSPO signals in the vicinity of the impact. Astrocytes also formed a TSPO-positive glial scar encompassing necrotic inflammation, and were clustered with PET-detectable TSPO signals in the bilateral external and internal capsules at late stages, putatively reacting with diffuse axonal injury. These observations support the applicability of TSPO-PET as an imaging-based preclinical and clinical biomarker assay in TBI, and indicate its potential capability to clarify aggressive and protective roles of glial responses to injury when combined with emerging anti-inflammatory and immunomodulatory treatments.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1557-9042
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1463-75
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pubmed:meshHeading |
pubmed-meshheading:20504160-Animals,
pubmed-meshheading:20504160-Autoradiography,
pubmed-meshheading:20504160-Brain Hemorrhage, Traumatic,
pubmed-meshheading:20504160-Fluorodeoxyglucose F18,
pubmed-meshheading:20504160-Gliosis,
pubmed-meshheading:20504160-Immunohistochemistry,
pubmed-meshheading:20504160-Male,
pubmed-meshheading:20504160-Mitochondrial ADP, ATP Translocases,
pubmed-meshheading:20504160-Nerve Regeneration,
pubmed-meshheading:20504160-Neuroglia,
pubmed-meshheading:20504160-Positron-Emission Tomography,
pubmed-meshheading:20504160-Radiopharmaceuticals,
pubmed-meshheading:20504160-Rats,
pubmed-meshheading:20504160-Rats, Wistar
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pubmed:year |
2010
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pubmed:articleTitle |
Glial cell-mediated deterioration and repair of the nervous system after traumatic brain injury in a rat model as assessed by positron emission tomography.
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pubmed:affiliation |
Molecular Imaging Center, National Institute of Radiological Sciences, Chiba, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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