@article{oai:repo.qst.go.jp:00047212,
 author = {Yu, Iwae and Inaji, Motoki and Maeda, Jun and Okauchi, Takashi and Nariai, Tadashi and Ohno, Kikuo and Higuchi, Makoto and Suhara, Tetsuya and 前田 純 and 樋口 真人 and 須原 哲也},
 issue = {8},
 journal = {Journal of neurotrauma},
 month = {Aug},
 note = {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.},
 pages = {1463--1475},
 title = {Glial cell-mediated deterioration and repair of the nervous system after traumatic brain injury in a rat model as assessed by positron emission tomography.},
 volume = {27},
 year = {2010}
}