Protein aggregation in Parkinson’s disease
Identifieur interne : 000833 ( Main/Corpus ); précédent : 000832; suivant : 000834Protein aggregation in Parkinson’s disease
Auteurs : V. GundersenSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 2010-07.
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Abstract
Gundersen V. Protein aggregation in Parkinson’s disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82–87. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson’s disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non‐dopaminergic neurons are known to be affected in Parkinsons’s disease, for example, in several brain stem nuclei and the olfactoric bulb (2–4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5–8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below.
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DOI: 10.1111/j.1600-0404.2010.01382.x
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Protein aggregation in Parkinson’s disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82–87. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson’s disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non‐dopaminergic neurons are known to be affected in Parkinsons’s disease, for example, in several brain stem nuclei and the olfactoric bulb (2–4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5–8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>V. Gundersen</name><affiliations><json:string>Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>alpha‐synuclein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>parkin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>proteasome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ubiquitin</value></json:item></subject><articleId><json:string>ANE1382</json:string></articleId><language><json:string>eng</json:string></language><abstract>Gundersen V. Protein aggregation in Parkinson’s disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82–87. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson’s disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non‐dopaminergic neurons are known to be affected in Parkinsons’s disease, for example, in several brain stem nuclei and the olfactoric bulb (2–4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5–8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. 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Protein aggregation in Parkinson’s disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82–87. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson’s disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non‐dopaminergic neurons are known to be affected in Parkinsons’s disease, for example, in several brain stem nuclei and the olfactoric bulb (2–4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5–8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>alpha‐synuclein</term></item><item><term>parkin</term></item><item><term>proteasome</term></item><item><term>ubiquitin</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/4A266E8D20487BEB87DF8CE0D5C4648835421CF6/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0404</doi><issn type="print">0001-6314</issn><issn type="electronic">1600-0404</issn><idGroup><id type="product" value="ANE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ACTA NEUROLOGICA SCANDINAVICA">Acta Neurologica Scandinavica</title></titleGroup></publicationMeta><publicationMeta level="part" position="07000"><doi origin="wiley">10.1111/ane.2010.122.issue-s190</doi><titleGroup><title type="specialIssueTitle">Selected Articles from the Annual Meeting of the Norwegian Neurological Association, Oslo, November 2009</title></titleGroup><numberingGroup><numbering type="journalVolume" number="122">122</numbering><numbering type="supplement">s190</numbering></numberingGroup><coverDate startDate="2010-07">July 2010</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="16" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.2010.01382.x</doi><idGroup><id type="unit" value="ANE1382"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Review Articles</title></titleGroup><copyright>© 2010 John Wiley & Sons A/S</copyright><eventGroup><event type="firstOnline" date="2010-06-02"></event><event type="publishedOnlineFinalForm" date="2010-06-02"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-06-03"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="82">82</numbering><numbering type="pageLast" number="87">87</numbering></numberingGroup><correspondenceTo>Vidar Gundersen, Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
Tel.: +47 22 85 14 96
Fax: +47 22 85 12 78
e‐mail: <email>vidar.gunderson@medisin.uio.no</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE1382.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Protein aggregation in Parkinson’s disease</title><title type="shortAuthors"><b>Gundersen</b></title><title type="short"><b>Protein aggregation in Parkinson’s disease</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>V.</givenNames><familyName>Gundersen</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="NO"><unparsedAffiliation>Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">alpha‐synuclein</keyword><keyword xml:id="k2">parkin</keyword><keyword xml:id="k3">proteasome</keyword><keyword xml:id="k4">ubiquitin</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Gundersen V. Protein aggregation in Parkinson’s disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82–87. © 2010 John Wiley & Sons A/S.</p><p>Parkinson’s disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson’s disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (<link href="#b1">1</link>). In addition, non‐dopaminergic neurons are known to be affected in Parkinsons’s disease, for example, in several brain stem nuclei and the olfactoric bulb (<link href="#b2 #b3 #b4">2–4</link>). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (<link href="#b5 #b6 #b7 #b8">5–8</link>), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1" numbered="no"><p>Conflicts of interest: none.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Protein aggregation in Parkinson’s disease</title></titleInfo><titleInfo type="abbreviated"><title>Protein aggregation in Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Protein aggregation in Parkinson’s disease</title></titleInfo><name type="personal"><namePart type="given">V.</namePart><namePart type="family">Gundersen</namePart><affiliation>Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-07</dateIssued><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Gundersen V. Protein aggregation in Parkinson’s disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82–87. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson’s disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non‐dopaminergic neurons are known to be affected in Parkinsons’s disease, for example, in several brain stem nuclei and the olfactoric bulb (2–4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5–8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below.</abstract><subject lang="en"><genre>Keywords</genre><topic>alpha‐synuclein</topic><topic>parkin</topic><topic>proteasome</topic><topic>ubiquitin</topic></subject><relatedItem type="host"><titleInfo><title>Acta Neurologica Scandinavica</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0001-6314</identifier><identifier type="eISSN">1600-0404</identifier><identifier type="DOI">10.1111/(ISSN)1600-0404</identifier><identifier type="PublisherID">ANE</identifier><part><date>2010</date><detail type="title"><title>Selected Articles from the Annual Meeting of the Norwegian Neurological Association, Oslo, November 2009</title></detail><detail type="volume"><caption>vol.</caption><number>122</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s190</number></detail><extent unit="pages"><start>82</start><end>87</end><total>6</total></extent></part></relatedItem><identifier type="istex">4A266E8D20487BEB87DF8CE0D5C4648835421CF6</identifier><identifier type="DOI">10.1111/j.1600-0404.2010.01382.x</identifier><identifier type="ArticleID">ANE1382</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 John Wiley & Sons A/S</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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