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dc.contributor.author | Tanaka, Seigo | en |
dc.contributor.author | Takehashi, Masanori | en |
dc.contributor.author | Matoh, Naomi | en |
dc.contributor.author | Ueda, Kunihiro | en |
dc.date.accessioned | 2008-08-25T06:21:37Z | - |
dc.date.available | 2008-08-25T06:21:37Z | - |
dc.date.issued | 2001-03 | - |
dc.identifier.issn | 1342-0321 | - |
dc.identifier.uri | http://hdl.handle.net/2433/65269 | - |
dc.description.abstract | α-Synuclein is implicated in pathogenesis of various neurodegenerative diseases, but the molecular mechanisms of its action might be different. In Alzheimer's disease (AD), NAC (non-Aβ component of AD amyloid) is produced from α-synuclein, and then interacts with A protein to form amyloid in senile plaques. In Parkinson's disease (PD) and Dementia with Lewy bodies (DLB), a full-length or partially truncated form of α-synuclein is a constituent of LB, that is an inclusion found in degenerating neurons. Recently, oligodendroglial cytoplasmic inclusion in multiple system atrophy was reported to be immunoreactive with anti-α-synuclein antibody. Therefore, α-synuclein is suggested to be a common mediator of neurodegenerative diseases. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Institute for Chemical Research, Kyoto University | en |
dc.subject | α-Synuclein | en |
dc.subject | Alzheimer's disease | en |
dc.subject | Parkinson's disease | en |
dc.subject | Amyloid | en |
dc.subject | Lewy body | en |
dc.subject.ndc | 430 | - |
dc.title | α-Synuclein and Neurodegeneration (BIOORGANIC CHEMISTRY-Molecular Clinical Chemistry) | en |
dc.type | article | - |
dc.type.niitype | Article | - |
dc.identifier.ncid | AA11061308 | - |
dc.identifier.jtitle | ICR Annual Report | en |
dc.identifier.volume | 7 | - |
dc.identifier.spage | 42 | - |
dc.identifier.epage | 43 | - |
dc.textversion | publisher | - |
dc.sortkey | 23 | - |
dcterms.accessRights | open access | - |
dc.identifier.pissn | 1342-0321 | - |
出現コレクション: | Vol.7 (2000) |
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