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dc.contributor.authorTanaka, Seigoen
dc.contributor.authorTakehashi, Masanorien
dc.contributor.authorMatoh, Naomien
dc.contributor.authorUeda, Kunihiroen
dc.date.accessioned2008-08-25T06:21:37Z-
dc.date.available2008-08-25T06:21:37Z-
dc.date.issued2001-03-
dc.identifier.issn1342-0321-
dc.identifier.urihttp://hdl.handle.net/2433/65269-
dc.description.abstractα-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.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherInstitute for Chemical Research, Kyoto Universityen
dc.subjectα-Synucleinen
dc.subjectAlzheimer's diseaseen
dc.subjectParkinson's diseaseen
dc.subjectAmyloiden
dc.subjectLewy bodyen
dc.subject.ndc430-
dc.titleα-Synuclein and Neurodegeneration (BIOORGANIC CHEMISTRY-Molecular Clinical Chemistry)en
dc.typearticle-
dc.type.niitypeArticle-
dc.identifier.ncidAA11061308-
dc.identifier.jtitleICR Annual Reporten
dc.identifier.volume7-
dc.identifier.spage42-
dc.identifier.epage43-
dc.textversionpublisher-
dc.sortkey23-
dcterms.accessRightsopen access-
dc.identifier.pissn1342-0321-
出現コレクション:Vol.7 (2000)

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