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Glial cell-mediated deterioration and repair of the nervous system after traumatic brain injury in a rat model as assessed by positron emission tomography.
https://repo.qst.go.jp/records/47212
https://repo.qst.go.jp/records/472120ed6d483-7daf-42e4-bbd4-a2518f058711
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2015-08-06 | |||||
タイトル | ||||||
タイトル | Glial cell-mediated deterioration and repair of the nervous system after traumatic brain injury in a rat model as assessed by positron emission tomography. | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
Yu, Iwae
× Yu, Iwae× Inaji, Motoki× Maeda, Jun× Okauchi, Takashi× Nariai, Tadashi× Ohno, Kikuo× Higuchi, Makoto× Suhara, Tetsuya× 前田 純× 樋口 真人× 須原 哲也 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 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. | |||||
書誌情報 |
Journal of neurotrauma 巻 27, 号 8, p. 1463-1475, 発行日 2010-08 |
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出版者 | ||||||
出版者 | Mary Ann Liebert | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0897-7151 | |||||
PubMed番号 | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 20504160 |