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Tau filaments and development of positron emission tomography (PET) tracers
https://repo.qst.go.jp/records/49046
https://repo.qst.go.jp/records/49046b46cf83d-d8f8-4958-a975-01ef44fe2363
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2018-05-18 | |||||
| タイトル | ||||||
| タイトル | Tau filaments and development of positron emission tomography (PET) tracers | |||||
| 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 |
Goedert, Michel
× Goedert, Michel× Yamaguchi, Yoshiki× K., Mishra Sushi× higuchi, Makoto× Sahara, Naruhiko× 樋口 真人× 佐原 成彦 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Neurofibrillary lesions strongly correlate with cognitive deficits, making them an important therapeutic target for Alzheimer’s disease (AD) (1, 2). Dominantly inherited mutations in MAPT, the Tau gene, cause a form of frontotemporal dementia that can be associated with parkinsonism (FTDP- 17T), showing that dysfunction of Tau protein is sufficient to cause neurodegeneration and dementia (3). In FTDP-17T, abundant filamentous Tau inclusions are present in either nerve cells or in both nerve cells and glial cells. Aβ deposits, a defining feature of AD, are not characteristic of FTDP-17T. However, there are many similarities between cases of FTDP-17T and other pure Tauopathies, such as sporadic progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), and Pick’s disease, especially with regard to the isoform composition of Tau filaments. |
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| 書誌情報 |
Frontiers in Neurology 巻 9, p. 70, 発行日 2018-02 |
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| PubMed番号 | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | 29497399 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.3389/fneur.2018.00070 | |||||
