シンポジウム8―3 パーキンソン病の臨床,基礎の最前線 パーキンソン病の病態:分子生物学からわかったこと
書誌事項
- タイトル別名
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- Cellular pathophysiology of Parkinson's disease
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To explore pathogenesis of synucleinopathy including Parkinson's disease and multiple system atrophy, we developed cellular model for synucleinopathy. In this experimental model, α-synuclein was overexpressed in SH-SY5Y cells, which were then exposed to mitochondrial toxins. The data thus obtained suggested the followings.<br> 1) By the treatment with rotenone, wild type α-synuclein overexpressing cells demonstrated intracellular aggregations, which shared a number of features with Lewy bodies.<br> 2) The aggregate formation of α-synuclein may be cytoprotective.<br> 3) The catechol-derived quinones are candidate molecules to facilitate the oligomer formation of α-synuclein.<br> 4) The cells overexpressing S129A mutant showed few aggregations. It is suggested that phosphorylation at serine 129 is essential for aggregate formation.<br> 5) In wild-type α-synuclein cells treated with rotenone, unfolded protein response (UPR) markers were induced prior to the induction of mitochondrial disruption and caspase-3 activation.<br> 6) On the other hand, the S129A mutant failed to activate these UPRs. Thus it seems plausible that α-synuclein toxicity is dependent on the phosphorylation at S129.<br>
収録刊行物
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- 臨床神経学
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臨床神経学 48 (11), 984-985, 2008
日本神経学会
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詳細情報 詳細情報について
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- CRID
- 1390282680012871424
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- NII論文ID
- 10024898757
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- NII書誌ID
- AN00253207
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- ISSN
- 18820654
- 0009918X
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- データソース種別
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- JaLC
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- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可