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Oxidative Stress and Neurodegeneration in Prion Diseases

Authors
 Jae-Il Kim  ;  Seung-Il Choi  ;  Nam-Ho Kim  ;  Jae-Kwang Jin  ;  Eun-Kyoung Choi  ;  Richard I. Carp  ;  Yong-Sun Kim 
Citation
 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.928 : 182-186, 2001 
Journal Title
 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 
ISSN
 0077-8923 
Issue Date
2001
MeSH
Animals ; Brain/metabolism ; Brain/pathology ; Gene Expression Regulation ; Humans ; Models, Biological ; NF-kappa B/metabolism ; Nerve Degeneration/metabolism* ; Nerve Tissue Proteins/metabolism ; Neuroglia/metabolism ; Neuroglia/pathology ; Neurons/metabolism* ; Neurons/pathology ; Oxidation-Reduction ; Oxidative Stress* ; PrPC Proteins/metabolism ; PrPSc Proteins/metabolism ; Prion Diseases/metabolism* ; Prion Diseases/pathology ; Reactive Oxygen Species/metabolism ; Scrapie/metabolism ; Scrapie/pathology ; Sheep ; Transcription, Genetic
Keywords
neurodegeneration ; oxidative stress ; prion disease
Abstract
Transmissible spongiform encephalopathies (TSEs), also termed prion diseases, are a group of fatal neurodegenerative diseases that affect humans and a number of other animal species. The etiology of these diseases is thought to be associated with the conversion of a normal protein, PrPC, into an infectious, pathogenic form, PrPSc. The PrPSc form shows greater protease resistance than PrPC and accumulates in affected individuals, often in the form of extracellular plaques. The pathogenesis and the molecular basis of neuronal cell death in these diseases are not well understood. Oxidative stress has been proposed to play an important role in the pathogenesis of several neurodegenerative disorders. In the present study, evidence of oxidative stress in scrapie, the archetype disease of the TSEs, is discussed. In addition, the mechanisms whereby oxidative stress could lead to neuronal degeneration are described.
Full Text
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2001.tb05648.x/abstract
DOI
10.1111/j.1749-6632.2001.tb05648.x
Appears in Collections:
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers
Yonsei Authors
Choi, Seung Il(최승일) ORCID logo https://orcid.org/0000-0001-7168-8795
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/142837
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