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α-Synuclein and Parkinson's disease. Takeshi IWATSUBO 1 1Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, University of Tokyo Keyword: α-synuclein , パーキンソン病 , Lewy小体 pp.569-576
Published Date 2000/8/10
DOI https://doi.org/10.11477/mf.1431901171
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The discovery of missense mutations in α-synuclein genes in some pedigrees of familial Parkinson's disease as well as the detection of a-synuclein protein in Lewy bodies of Parkinson's disease and dementia with Lewy bodies strongly implicated aggregation of a-synuclein in the pathogenesis of these neurodegenerative disorders. Very recently, transgenic animals overexpressing a-synuclein and exhibiting Parkinson-like phenotypes were generated. Notably, transgenic flies overexpressing wild-type or mutant human α-synuclein showed selective degeneration of a subset of dopamine neurons, α-synuclein-positive neuronal inclusions highly remniscent of human Lewy bodies, and motor deficit. Further genetic and cell biological analyses using these animal models will facilitate the elucidation of the pathogenetic mechanism whereby abnormal aggregation of α-synuclein leads to neuronal death in Parkinson's disease.


Copyright © 2000, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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