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Imaging distinct strains of tau fibrils in Alzheimer's disease and related neurodegenerative disorders
https://repo.qst.go.jp/records/73222
https://repo.qst.go.jp/records/73222fb8a4701-9897-4ba7-87f0-e2f08615847d
Item type | 会議発表用資料 / Presentation(1) | |||||
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公開日 | 2014-12-02 | |||||
タイトル | ||||||
タイトル | Imaging distinct strains of tau fibrils in Alzheimer's disease and related neurodegenerative disorders | |||||
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 |
Higuchi, Makoto
× Higuchi, Makoto× Shimada, Hitoshi× Sahara, Naruhiko× Maruyama, Masahiro× Shinotoh, Hitoshi× Ming-Rong, Zhang× Suhara, Tetsuya× Higuchi, Makoto× Shimada, Hitoshi× Sahara, Naruhiko× Maruyama, Masahiro× Shinoto, Hitoshi× Ming-Rong, Zhang× Suhara, Tetsuya |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Deposition of fibrillary tau aggregates in the brain is characteristic of Alzheimer’s disease (AD) and allied disorders including frontotemporal lobar degeneration (FTLD), and has been reported to be tightly associated with neuronal loss in these illnesses. We recently developed an imaging agent, PBB3, applicable to positron emission tomography (PET) for humans and transgenic mouse models of tau pathologies. Preclinical and clinical PET studies have demonstrated that PBB3 retention in the brain reflects tau deposition in AD and familial and sporadic FTLDs. Our results have also supported the utility of PBB3-PET as an objective index for progression of AD, and have indicated that PBB3-positive tau deposition may precede reduction of regional cerebral glucose metabolism in transition from prodromal to severe AD. Notably, PET images of diverse tau-positive diseases highlight the view that isoform composition, mutation and even minor fibril strains of tau could determine mechanisms of tau-induced neurotoxicity, reactivity of tau with PET ligands and subcellular and regional localizations of pathological tau assemblies. Hence, reactivity with PBB3 and other PET ligands would help to identify a tau strain accumulating in each individual, facilitating a strain-specific anti-tau therapy as personalized medicine. Finally, 18F-fluorinated PBB3 derivatives with a longer radioactive half-life are being developed for wider availability and better dynamic range, potentially offering robust clarification of roles played by distinct tau fibril strains in neurodegeneration. | |||||
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 | Brain Conference 2014 | |||||
発表年月日 | ||||||
日付 | 2014-11-07 | |||||
日付タイプ | Issued |