Role of Mitochondria in Parkinson Disease
Identifieur interne : 000113 ( Main/Corpus ); précédent : 000112; suivant : 000114Role of Mitochondria in Parkinson Disease
Auteurs : S. Kösel ; G. Hofhaus ; A. Maassen ; P. Vieregge ; M. B. GraeberSource :
- Biological Chemistry [ 1431-6730 ] ; 1999-07-01.
Abstract
The cause of the selective degeneration of nigrostriatal neurons in Parkinson disease (PD) has remained largely unknown. Exceptions include rare missense mutations in the alpha-synuclein gene on chromosome 4, a potentially pathogenic mutation affecting the ubiquitin pathway, and mutations in the parkin gene on chromosome 6. However, unlike classical PD, the latter syndrome is not associated with the formation of typical Lewy bodies. In contrast, a biochemical defect of complex I of the mitochondrial respiratory chain has been described in a relatively large group of confirmed PD cases. Recent cybrid studies indicate that the complex I defect in PD has a genetic cause and that it may arise from mutations in the mitochondrial DNA. Sequence analysis of the mitochondrial genome supports the view that mitochondrial point mutations are involved in PD pathogenesis. However, although mitochondria function as regulators in several known forms of cell death, their exact involvement in PD has remained unresolved. This is of relevance because classical apoptosis does not appear to play a major role in the degeneration of the parkinsonian nigra.
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DOI: 10.1515/BC.1999.106
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Exceptions include rare missense mutations in the alpha-synuclein gene on chromosome 4, a potentially pathogenic mutation affecting the ubiquitin pathway, and mutations in the parkin gene on chromosome 6. However, unlike classical PD, the latter syndrome is not associated with the formation of typical Lewy bodies. In contrast, a biochemical defect of complex I of the mitochondrial respiratory chain has been described in a relatively large group of confirmed PD cases. Recent cybrid studies indicate that the complex I defect in PD has a genetic cause and that it may arise from mutations in the mitochondrial DNA. Sequence analysis of the mitochondrial genome supports the view that mitochondrial point mutations are involved in PD pathogenesis. However, although mitochondria function as regulators in several known forms of cell death, their exact involvement in PD has remained unresolved. 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In contrast, a biochemical defect of complex I of the mitochondrial respiratory chain has been described in a relatively large group of confirmed PD cases. Recent cybrid studies indicate that the complex I defect in PD has a genetic cause and that it may arise from mutations in the mitochondrial DNA. Sequence analysis of the mitochondrial genome supports the view that mitochondrial point mutations are involved in PD pathogenesis. However, although mitochondria function as regulators in several known forms of cell death, their exact involvement in PD has remained unresolved. 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B.</given-names><x> </x><surname>Graeber</surname></name></contrib></contrib-group><pub-date pub-type="ppub"><day>01</day><month>07</month><year>1999</year><string-date>July 1999</string-date></pub-date><pub-date pub-type="epub"><day>01</day><month>06</month><year>2005</year></pub-date><volume>380</volume><issue>7-8</issue><fpage seq="16">865</fpage><lpage>870</lpage><copyright-statement>Copyright © 1999 by Walter de Gruyter GmbH & Co. KG</copyright-statement><copyright-year>1999</copyright-year><related-article related-article-type="pdf" xlink:href="bc.1999.106.pdf"></related-article><abstract><title>Abstract</title><p>The cause of the selective degeneration of nigrostriatal neurons in Parkinson disease (PD) has remained largely unknown. Exceptions include rare missense mutations in the alpha-synuclein gene on chromosome 4, a potentially pathogenic mutation affecting the ubiquitin pathway, and mutations in the parkin gene on chromosome 6. However, unlike classical PD, the latter syndrome is not associated with the formation of typical Lewy bodies. In contrast, a biochemical defect of complex I of the mitochondrial respiratory chain has been described in a relatively large group of confirmed PD cases. Recent cybrid studies indicate that the complex I defect in PD has a genetic cause and that it may arise from mutations in the mitochondrial DNA. Sequence analysis of the mitochondrial genome supports the view that mitochondrial point mutations are involved in PD pathogenesis. However, although mitochondria function as regulators in several known forms of cell death, their exact involvement in PD has remained unresolved. This is of relevance because classical apoptosis does not appear to play a major role in the degeneration of the parkinsonian nigra.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of Mitochondria in Parkinson Disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Role of Mitochondria in Parkinson Disease</title></titleInfo><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Kösel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Hofhaus</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Maassen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Vieregge</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. B.</namePart><namePart type="family">Graeber</namePart><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article"></genre><subject><genre>subject</genre><topic authority="JournalSubjectCodes" authorityURI="PSB">Biochemistry</topic><topic authority="JournalSubjectCodes" authorityURI="PSD">Molecular biology</topic><topic authority="JournalSubjectCodes" authorityURI="PSF">Cellular biology</topic></subject><originInfo><publisher>Walter de Gruyter</publisher><dateIssued encoding="w3cdtf">1999-07-01</dateIssued><dateCreated encoding="w3cdtf">2005-06-01</dateCreated><copyrightDate encoding="w3cdtf">1999</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The cause of the selective degeneration of nigrostriatal neurons in Parkinson disease (PD) has remained largely unknown. Exceptions include rare missense mutations in the alpha-synuclein gene on chromosome 4, a potentially pathogenic mutation affecting the ubiquitin pathway, and mutations in the parkin gene on chromosome 6. However, unlike classical PD, the latter syndrome is not associated with the formation of typical Lewy bodies. In contrast, a biochemical defect of complex I of the mitochondrial respiratory chain has been described in a relatively large group of confirmed PD cases. Recent cybrid studies indicate that the complex I defect in PD has a genetic cause and that it may arise from mutations in the mitochondrial DNA. Sequence analysis of the mitochondrial genome supports the view that mitochondrial point mutations are involved in PD pathogenesis. However, although mitochondria function as regulators in several known forms of cell death, their exact involvement in PD has remained unresolved. This is of relevance because classical apoptosis does not appear to play a major role in the degeneration of the parkinsonian nigra.</abstract><relatedItem type="host"><titleInfo><title>Biological Chemistry</title></titleInfo><titleInfo type="abbreviated"><title>Biological Chemistry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1431-6730</identifier><identifier type="PublisherID">bchm</identifier><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>380</number></detail><detail type="issue"><caption>no.</caption><number>7-8</number></detail><extent unit="pages"><start>865</start><end>870</end></extent></part></relatedItem><relatedItem type="reviewOf"><genre>pdf</genre><identifier type="pdf">bc.1999.106.pdf</identifier></relatedItem><identifier type="istex">01E05AF8941EB95AD56AA6D19B332E5AF63440A7</identifier><identifier type="DOI">10.1515/BC.1999.106</identifier><identifier type="ArticleID">bchm.380.7-8.865</identifier><identifier type="Related-article-Href">bc.1999.106.pdf</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1999 by Walter de Gruyter GmbH & Co. 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