Mitochondrial dysfunction in parkinson's disease
Identifieur interne : 001A40 ( Main/Corpus ); précédent : 001A39; suivant : 001A41Mitochondrial dysfunction in parkinson's disease
Auteurs : Mizuno ; Hiroyo Yoshino ; Shin-Ichiro Ikebe ; Nobutaka Hattori ; Tomonori Kobayashi ; Satoe Shimoda-Matsubayashi ; Hiroto Matsumine ; Tomoyoshi KondoSource :
- Annals of Neurology [ 0364-5134 ] ; 1998-09.
Abstract
This review discusses the etiology and pathogenesis of Parkinson's disease (PD). Mitochondrial respiratory failure and oxidative stress appear to be two major contributors to nigral neuronal death in PD. Complex I deficiency has been reported by several groups and appears to be one of the basic abnormalities responsible for mitochondrial failure. The principal question is whether or not complex I deficiency is primary or secondary. The second question is whether or not complex I deficiency is localized in the nigrostriatal system or is systemically present. It is our impression that complex I deficiency is not the primary cause but that its deficiency appears to be systemic. The primary cause may be the combination of genetic background and potential nigral neurotoxins. Exposure of nigral neurons to a high risk for oxidative damage because of its high dopamine content may be the reason for more pronounced nigral complex I deficiency compared to systemic organs. Oxidative stress and mitochondrial failure produce a vicious cycle in nigral neurons. To explore the genetic risk factors of sporadic PD, studies on familial PD and parkinsonism are important. Recently, an autosomal dominant form of familial PD was found to be caused by point mutations of the α‐synuclein gene, and an autosomal recessive familial parkinsonism was mapped to the long arm of chromosome 6 near the Mn‐SOD gene locus. Information obtained in these familial cases will contribute to the research on sporadic PD.
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DOI: 10.1002/ana.410440715
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Matsumine</name><affiliation><mods:affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kondo, Tomoyoshi" sort="Kondo, Tomoyoshi" uniqKey="Kondo T" first="Tomoyoshi" last="Kondo">Tomoyoshi Kondo</name><affiliation><mods:affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-09">1998-09</date><biblScope unit="volume">44</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="supplement">1</biblScope><biblScope unit="page" from="S99">S99</biblScope><biblScope 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Mitochondrial respiratory failure and oxidative stress appear to be two major contributors to nigral neuronal death in PD. Complex I deficiency has been reported by several groups and appears to be one of the basic abnormalities responsible for mitochondrial failure. The principal question is whether or not complex I deficiency is primary or secondary. The second question is whether or not complex I deficiency is localized in the nigrostriatal system or is systemically present. It is our impression that complex I deficiency is not the primary cause but that its deficiency appears to be systemic. The primary cause may be the combination of genetic background and potential nigral neurotoxins. Exposure of nigral neurons to a high risk for oxidative damage because of its high dopamine content may be the reason for more pronounced nigral complex I deficiency compared to systemic organs. Oxidative stress and mitochondrial failure produce a vicious cycle in nigral neurons. To explore the genetic risk factors of sporadic PD, studies on familial PD and parkinsonism are important. Recently, an autosomal dominant form of familial PD was found to be caused by point mutations of the α‐synuclein gene, and an autosomal recessive familial parkinsonism was mapped to the long arm of chromosome 6 near the Mn‐SOD gene locus. Information obtained in these familial cases will contribute to the research on sporadic PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr Mizuno MD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Hiroyo Yoshino BS</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Shin‐Ichiro Ikebe MD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Nobutaka Hattori MD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Tomonori Kobayashi MD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Satoe Shimoda‐Matsubayashi MD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Hiroto Matsumine MD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Tomoyoshi Kondo MD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item></author><articleId><json:string>ANA410440715</json:string></articleId><language><json:string>eng</json:string></language><abstract>This review discusses the etiology and pathogenesis of Parkinson's disease (PD). Mitochondrial respiratory failure and oxidative stress appear to be two major contributors to nigral neuronal death in PD. Complex I deficiency has been reported by several groups and appears to be one of the basic abnormalities responsible for mitochondrial failure. The principal question is whether or not complex I deficiency is primary or secondary. The second question is whether or not complex I deficiency is localized in the nigrostriatal system or is systemically present. It is our impression that complex I deficiency is not the primary cause but that its deficiency appears to be systemic. The primary cause may be the combination of genetic background and potential nigral neurotoxins. Exposure of nigral neurons to a high risk for oxidative damage because of its high dopamine content may be the reason for more pronounced nigral complex I deficiency compared to systemic organs. Oxidative stress and mitochondrial failure produce a vicious cycle in nigral neurons. To explore the genetic risk factors of sporadic PD, studies on familial PD and parkinsonism are important. Recently, an autosomal dominant form of familial PD was found to be caused by point mutations of the α‐synuclein gene, and an autosomal recessive familial parkinsonism was mapped to the long arm of chromosome 6 near the Mn‐SOD gene locus. 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Mitochondrial respiratory failure and oxidative stress appear to be two major contributors to nigral neuronal death in PD. Complex I deficiency has been reported by several groups and appears to be one of the basic abnormalities responsible for mitochondrial failure. The principal question is whether or not complex I deficiency is primary or secondary. The second question is whether or not complex I deficiency is localized in the nigrostriatal system or is systemically present. It is our impression that complex I deficiency is not the primary cause but that its deficiency appears to be systemic. The primary cause may be the combination of genetic background and potential nigral neurotoxins. Exposure of nigral neurons to a high risk for oxidative damage because of its high dopamine content may be the reason for more pronounced nigral complex I deficiency compared to systemic organs. Oxidative stress and mitochondrial failure produce a vicious cycle in nigral neurons. To explore the genetic risk factors of sporadic PD, studies on familial PD and parkinsonism are important. Recently, an autosomal dominant form of familial PD was found to be caused by point mutations of the α‐synuclein gene, and an autosomal recessive familial parkinsonism was mapped to the long arm of chromosome 6 near the Mn‐SOD gene locus. 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type="main">Abstract</title><p>This review discusses the etiology and pathogenesis of Parkinson's disease (PD). Mitochondrial respiratory failure and oxidative stress appear to be two major contributors to nigral neuronal death in PD. Complex I deficiency has been reported by several groups and appears to be one of the basic abnormalities responsible for mitochondrial failure. The principal question is whether or not complex I deficiency is primary or secondary. The second question is whether or not complex I deficiency is localized in the nigrostriatal system or is systemically present. It is our impression that complex I deficiency is not the primary cause but that its deficiency appears to be systemic. The primary cause may be the combination of genetic background and potential nigral neurotoxins. Exposure of nigral neurons to a high risk for oxidative damage because of its high dopamine content may be the reason for more pronounced nigral complex I deficiency compared to systemic organs. Oxidative stress and mitochondrial failure produce a vicious cycle in nigral neurons. To explore the genetic risk factors of sporadic PD, studies on familial PD and parkinsonism are important. Recently, an autosomal dominant form of familial PD was found to be caused by point mutations of the α‐synuclein gene, and an autosomal recessive familial parkinsonism was mapped to the long arm of chromosome 6 near the Mn‐SOD gene locus. Information obtained in these familial cases will contribute to the research on sporadic PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mitochondrial dysfunction in parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Mitochondrial Dysfunction</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mitochondrial dysfunction in parkinson's disease</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr</namePart><namePart type="family">Mizuno</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><description>Correspondence: Department of Neurology, Juntendo University School of Medicine, 2‐1‐1 Hongo, Bunkyo, Tokyo 113, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroyo</namePart><namePart type="family">Yoshino</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shin‐Ichiro</namePart><namePart type="family">Ikebe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nobutaka</namePart><namePart type="family">Hattori</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomonori</namePart><namePart type="family">Kobayashi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Satoe</namePart><namePart type="family">Shimoda‐Matsubayashi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroto</namePart><namePart type="family">Matsumine</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomoyoshi</namePart><namePart type="family">Kondo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-09</dateIssued><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">3</extent><extent unit="tables">3</extent></physicalDescription><abstract lang="en">This review discusses the etiology and pathogenesis of Parkinson's disease (PD). Mitochondrial respiratory failure and oxidative stress appear to be two major contributors to nigral neuronal death in PD. Complex I deficiency has been reported by several groups and appears to be one of the basic abnormalities responsible for mitochondrial failure. The principal question is whether or not complex I deficiency is primary or secondary. The second question is whether or not complex I deficiency is localized in the nigrostriatal system or is systemically present. It is our impression that complex I deficiency is not the primary cause but that its deficiency appears to be systemic. The primary cause may be the combination of genetic background and potential nigral neurotoxins. Exposure of nigral neurons to a high risk for oxidative damage because of its high dopamine content may be the reason for more pronounced nigral complex I deficiency compared to systemic organs. Oxidative stress and mitochondrial failure produce a vicious cycle in nigral neurons. To explore the genetic risk factors of sporadic PD, studies on familial PD and parkinsonism are important. Recently, an autosomal dominant form of familial PD was found to be caused by point mutations of the α‐synuclein gene, and an autosomal recessive familial parkinsonism was mapped to the long arm of chromosome 6 near the Mn‐SOD gene locus. Information obtained in these familial cases will contribute to the research on sporadic PD.</abstract><note type="funding">Grant‐in‐Aid for Scientific Research on Priority Areas and by a Grant‐in‐Aid for Neuroscience Research from Ministry of Education, Science and Culture, Japan</note><note type="funding">Center of Excellence Grant from the National Parkinson Foundation, Miami</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>44</number></detail><detail type="issue"><caption>no.</caption><number>S1</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>1</number></detail><extent unit="pages"><start>S99</start><end>S109</end><total>11</total></extent></part></relatedItem><identifier type="istex">77DE88A4977ED01E51E819C5FD804CE339133B5A</identifier><identifier type="DOI">10.1002/ana.410440715</identifier><identifier type="ArticleID">ANA410440715</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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