Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
Identifieur interne : 001490 ( Main/Corpus ); précédent : 001489; suivant : 001491Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
Auteurs : Michael T. Lin ; M. Flint BealSource :
- Nature [ 0028-0836 ] ; 2006-10-19.
Abstract
Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.
Url:
DOI: 10.1038/nature05292
Links to Exploration step
ISTEX:0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BBLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</title><author><name sortKey="Lin, Michael T" sort="Lin, Michael T" uniqKey="Lin M" first="Michael T." last="Lin">Michael T. Lin</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</mods:affiliation></affiliation></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: fbeal@med.cornell.edu</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1038/nature05292</idno><idno type="url">https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001490</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</title><author><name sortKey="Lin, Michael T" sort="Lin, Michael T" uniqKey="Lin M" first="Michael T." last="Lin">Michael T. Lin</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</mods:affiliation></affiliation></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: fbeal@med.cornell.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Nature</title><idno type="ISSN">0028-0836</idno><idno type="eISSN">1476-4687</idno><imprint><publisher>Nature Publishing Group</publisher><date type="published" when="2006-10-19">2006-10-19</date><biblScope unit="volume">443</biblScope><biblScope unit="issue">7113</biblScope><biblScope unit="page" from="787">787</biblScope><biblScope unit="page" to="795">795</biblScope></imprint><idno type="ISSN">0028-0836</idno></series><idno type="istex">0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB</idno><idno type="DOI">10.1038/nature05292</idno><idno type="ArticleID">nature05292</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0028-0836</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.</div></front></TEI><istex><corpusName>nature</corpusName><author><json:item><name>Michael T. Lin</name><affiliations><json:string>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</json:string></affiliations></json:item><json:item><name>M. Flint Beal</name><affiliations><json:string>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</json:string><json:string>E-mail: fbeal@med.cornell.edu</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.</abstract><qualityIndicators><score>6.236</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>790</abstractCharCount><pdfWordCount>8354</pdfWordCount><pdfCharCount>57472</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>103</abstractWordCount></qualityIndicators><title>Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</title><genre><json:string>research-article</json:string></genre><host><volume>443</volume><pages><total>9</total><last>795</last><first>787</first></pages><issn><json:string>0028-0836</json:string></issn><issue>7113</issue><genre><json:string>Insight</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1476-4687</json:string></eissn><title>Nature</title></host><categories><wos><json:string>MULTIDISCIPLINARY SCIENCES</json:string></wos></categories><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1038/nature05292</json:string></doi><id>0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Nature Publishing Group</publisher><availability><p>NATURE</p></availability><date>2006-10-18</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</title><author><persName><forename type="first">Michael T.</forename><surname>Lin</surname></persName><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</affiliation></author><author><persName><forename type="first">M. Flint</forename><surname>Beal</surname></persName><email>fbeal@med.cornell.edu</email><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</affiliation></author></analytic><monogr><title level="j">Nature</title><idno type="pISSN">0028-0836</idno><idno type="eISSN">1476-4687</idno><imprint><publisher>Nature Publishing Group</publisher><date type="published" when="2006-10-19"></date><biblScope unit="volume">443</biblScope><biblScope unit="issue">7113</biblScope><biblScope unit="page" from="787">787</biblScope><biblScope unit="page" to="795">795</biblScope></imprint></monogr><idno type="istex">0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB</idno><idno type="DOI">10.1038/nature05292</idno><idno type="ArticleID">nature05292</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006-10-18</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.</p></abstract></profileDesc><revisionDesc><change when="2006-10-18">Created</change><change when="2006-10-19">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus nature" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0"</istex:xmlDeclaration><istex:docType PUBLIC="-//NPG//DTD XML Article//EN" URI="NPG_XML_Article.dtd" name="istex:docType"><istex:entity PUBLIC="-//NatureAmerica//FICI nature05292-f1//EN" URL="//snapple/web_d/web/npg/nature/journal/v443/n7113/images/nature05292-f1.2.jpg" NDATA="ITEM" name="figf1"></istex:entity><istex:entity PUBLIC="-//NatureAmerica//FICI nature05292-f2//EN" URL="//snapple/web_d/web/npg/nature/journal/v443/n7113/images/nature05292-f2.2.jpg" NDATA="ITEM" name="figf2"></istex:entity><istex:entity PUBLIC="-//NatureAmerica//FICI nature05292-f3//EN" URL="//snapple/web_d/web/npg/nature/journal/v443/n7113/images/nature05292-f3.2.jpg" NDATA="ITEM" name="figf3"></istex:entity><istex:entity PUBLIC="-//NatureAmerica//FICI nature05292-t1//EN" URL="//snapple/web_d/web/npg/nature/journal/v443/n7113/images/nature05292-t1.jpg" NDATA="ITEM" name="tbl1"></istex:entity><istex:entity PUBLIC="-//NatureAmerica//FICI nature05292-t2//EN" URL="//snapple/web_d/web/npg/nature/journal/v443/n7113/images/nature05292-t2.jpg" NDATA="ITEM" name="tbl2"></istex:entity></istex:docType><istex:document><article id="nature05292" language="eng" publish="issue" relation="no" origsrc="yes"><pubfm><jtl>Nature</jtl><vol>443</vol><iss>7113</iss><idt>20061019</idt><categ id="categtxt"></categ><categtxt>Insight</categtxt><subcateg id="subcatxt"></subcateg><subcatxt>Review Article</subcatxt><pp><spn>787</spn><epn>795</epn><cnt>9</cnt></pp><issn type="print">0028-0836</issn><issn type="electronic">1476-4687</issn><cpg><cpy>2006</cpy><cpn>Nature Publishing Group</cpn></cpg><doi>10.1038/nature05292</doi></pubfm><fm><atl>Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</atl><aug><au><fnm>Michael T.</fnm><snm>Lin</snm><inits>M T</inits><orf rid="a1"></orf></au><cau><fnm>M. Flint</fnm><snm>Beal</snm><inits>M F</inits><orf rid="a1"></orf><corf rid="c1"></corf></cau><aff><oid id="a1"></oid><i>Department of Neurology and Neuroscience, Weill Medical College of Cornell University</i>, <street>Room F-610, 525 East 68th Street</street>, <cty>New York</cty> <zip>10021</zip>, <cny>USA</cny>.</aff><caff><coid id="c1"></coid><email>fbeal@med.cornell.edu</email></caff></aug><hst><pubdate type="iss" year="2006" month="10" day="18"></pubdate></hst><abs><p>Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.</p></abs></fm></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="eng"><title>Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</title></titleInfo><titleInfo type="alternative" lang="eng" contentType="CDATA"><title>Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases</title></titleInfo><name type="personal"><namePart type="given">Michael T.</namePart><namePart type="family">Lin</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. Flint</namePart><namePart type="family">Beal</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York 10021, USA.</affiliation><affiliation>E-mail: fbeal@med.cornell.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel=""></genre><originInfo><publisher>Nature Publishing Group</publisher><dateIssued encoding="w3cdtf">2006-10-19</dateIssued><dateCreated encoding="w3cdtf">2006-10-18</dateCreated><copyrightDate encoding="w3cdtf">2006</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="eng">Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.</abstract><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><genre type="Journal" displayLabel="Insight"></genre><identifier type="ISSN">0028-0836</identifier><identifier type="eISSN">1476-4687</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>443</number></detail><detail type="issue"><caption>no.</caption><number>7113</number></detail><extent unit="pages"><start>787</start><end>795</end><total>9</total></extent></part></relatedItem><identifier type="istex">0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB</identifier><identifier type="DOI">10.1038/nature05292</identifier><identifier type="ArticleID">nature05292</identifier><accessCondition type="use and reproduction" contentType="copyright">©2006 Nature Publishing Group</accessCondition><recordInfo><recordContentSource>NATURE</recordContentSource></recordInfo></mods></metadata><covers><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/covers/jpeg</uri></json:item></covers><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/annexes/jpeg</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">MULTIDISCIPLINARY SCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001490 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 001490 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:0EDB7C8FAAF69E8ECDC9E9AEE685D54F72D4B7BB
|texte= Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
}}
| This area was generated with Dilib version V0.6.23. |  |