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PET imaging of glial activation and neuroinflammation by positron-labeled TSPO ligands

https://repo.qst.go.jp/records/65161
https://repo.qst.go.jp/records/65161
e30cbf3a-6149-4a6f-a87c-eef811b1db4f
Item type 会議発表用資料 / Presentation(1)
公開日 2013-09-28
タイトル
タイトル PET imaging of glial activation and neuroinflammation by positron-labeled TSPO ligands
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_c94f
資源タイプ conference object
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 Maeda, Jun

× Maeda, Jun

WEKO 642050

Maeda, Jun

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前田 純

× 前田 純

WEKO 642051

en 前田 純

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内容記述タイプ Abstract
内容記述 Translocator protein-18kDa (TSPO) has been reported as peripheral benzodiazepine receptor (PBR), peripheral tissues-enriched benzodiazepine binding site. TSPO mainly locates on the mitochondrial outer membrane as a component of mitochondrial permeability transition pore (mPTP), and plays pivotal role in incorporation of cholesterol and protoporphyrin. The expression of TSPOs in the normal brain is kept low level, whereas is dramatically increased by ischemia, traumatic brain injury (TBI) and neuroinflammation. This phenomenon is interpreted as proliferation of microglia, but the reason for the increased in TSPO expression was little-known. My laboratory has clarified these questions by PET and immunohistochemistry techniques. [11C]DAA1106, [18F]Fluoroethyl-DAA1106 and [11C]AC-5216, novel developed TSPO PET ligands by our laboratory, visualize the elevated TSPO signal by neuroinflammation. In chemical brain injury model with ethanol microinjection, the proliferation of microglia and TSPO signal around the focus began to increase from 3 days and peaked at 7 days after injury. Immunohistochemical stains presented that the up-regulation of TSPO signal was observed in not only proliferated microglia but also astrocyte. In addition, examined in models of various AD and non-AD neuropathologies, revealing the following reactive glial dynamics underlying differential TSPO upregulation: (1) TSPO-negative astrogliosis uncoupled with microgliosis or coupled with TSPO -positive microgliosis associated with irreversible neuronal insults; (2) TSPO -positive astrogliosis coupled with TSPO negative microgliosis associated with minimal or reversible neuronal toxicity; and (3) the elevation of TSPO signal is markedly higher around the tauopathy and neuritic plaque than the diffuse plaque in the postmortem brain. Collecting these results, the TSPO signal up-regulation in AD responds to cell death-stimulus, and TSPO PET imaging is beneficial method for prediction of deleterious change evoked by neuroinflammation.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 二国間交流事業セミナー
発表年月日
日付 2013-09-20
日付タイプ Issued
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