Milestones in Parkinson's disease—Clinical and pathologic features
Identifieur interne : 000565 ( Istex/Corpus ); précédent : 000564; suivant : 000566Milestones in Parkinson's disease—Clinical and pathologic features
Auteurs : Glenda Halliday ; Andrew Lees ; Matthew SternSource :
- Movement Disorders [ 0885-3185 ] ; 2011-05.
English descriptors
Abstract
The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23669
Links to Exploration step
ISTEX:D3143478950ED27D311D670FCE4BA2216869276BLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Milestones in Parkinson's disease—Clinical and pathologic features</title><author><name sortKey="Halliday, Glenda" sort="Halliday, Glenda" uniqKey="Halliday G" first="Glenda" last="Halliday">Glenda Halliday</name><affiliation><mods:affiliation>Neuroscience Research Australia and the University of New South Wales, Sydney, Australia</mods:affiliation></affiliation></author><author><name sortKey="Lees, Andrew" sort="Lees, Andrew" uniqKey="Lees A" first="Andrew" last="Lees">Andrew Lees</name><affiliation><mods:affiliation>University College London, Reta Lila Weston Institute of Neurological Studies, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name><affiliation><mods:affiliation>University of Pennsylvania Health Systems, Pennsylvania Hospital, Department of Neurology, Philadelphia, Pennsylvania, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:D3143478950ED27D311D670FCE4BA2216869276B</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23669</idno><idno type="url">https://api.istex.fr/document/D3143478950ED27D311D670FCE4BA2216869276B/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000565</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Milestones in Parkinson's disease—Clinical and pathologic features</title><author><name sortKey="Halliday, Glenda" sort="Halliday, Glenda" uniqKey="Halliday G" first="Glenda" last="Halliday">Glenda Halliday</name><affiliation><mods:affiliation>Neuroscience Research Australia and the University of New South Wales, Sydney, Australia</mods:affiliation></affiliation></author><author><name sortKey="Lees, Andrew" sort="Lees, Andrew" uniqKey="Lees A" first="Andrew" last="Lees">Andrew Lees</name><affiliation><mods:affiliation>University College London, Reta Lila Weston Institute of Neurological Studies, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name><affiliation><mods:affiliation>University of Pennsylvania Health Systems, Pennsylvania Hospital, Department of Neurology, Philadelphia, Pennsylvania, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-05">2011-05</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1015">1015</biblScope><biblScope unit="page" to="1021">1021</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">D3143478950ED27D311D670FCE4BA2216869276B</idno><idno type="DOI">10.1002/mds.23669</idno><idno type="ArticleID">MDS23669</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Lewy bodies</term><term>neuropathology</term><term>preclinical Parkinson's disease</term><term>α‐synuclein</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Glenda Halliday PhD</name><affiliations><json:string>Neuroscience Research Australia and the University of New South Wales, Sydney, Australia</json:string></affiliations></json:item><json:item><name>Andrew Lees MD, FRCP</name><affiliations><json:string>University College London, Reta Lila Weston Institute of Neurological Studies, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Matthew Stern MD</name><affiliations><json:string>University of Pennsylvania Health Systems, Pennsylvania Hospital, Department of Neurology, Philadelphia, Pennsylvania, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>α‐synuclein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Lewy bodies</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuropathology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>preclinical Parkinson's disease</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.502</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1454</abstractCharCount><pdfWordCount>4910</pdfWordCount><pdfCharCount>31865</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>216</abstractWordCount></qualityIndicators><title>Milestones in Parkinson's disease—Clinical and pathologic features</title><genre><json:string>Serial article</json:string></genre><host><volume>26</volume><pages><total>7</total><last>1021</last><first>1015</first></pages><issn><json:string>0885-3185</json:string></issn><issue>6</issue><subject><json:item><value>Review</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23669</json:string></doi><id>D3143478950ED27D311D670FCE4BA2216869276B</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/D3143478950ED27D311D670FCE4BA2216869276B/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/D3143478950ED27D311D670FCE4BA2216869276B/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/D3143478950ED27D311D670FCE4BA2216869276B/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Milestones in Parkinson's disease—Clinical and pathologic features</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Relevant conflicts of interest/financial disclosures: Glenda Halliday is a Senior Principal Research Fellowship of the National Health and Medical Research Council of Australia (fellowship #350827). Andrew Lees receives funding from the Weston Trust and the PSP (Europe) Association. Matthew Stern is a consultant to Teva, Medtronic, Ipsen, Schering‐Plough, Adamas, and Novartis.Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Milestones in Parkinson's disease—Clinical and pathologic features</title><author><persName><forename type="first">Glenda</forename><surname>Halliday</surname><roleName type="degree">PhD</roleName></persName><affiliation>Neuroscience Research Australia and the University of New South Wales, Sydney, Australia</affiliation></author><author><persName><forename type="first">Andrew</forename><surname>Lees</surname><roleName type="degree">MD, FRCP</roleName></persName><note type="correspondence"><p>Correspondence: University College London, Reta Lila Weston Institute of Neurological Studies, 1 Wakefield Street, London WC1N 1PJ, UK</p></note><affiliation>University College London, Reta Lila Weston Institute of Neurological Studies, London, United Kingdom</affiliation></author><author><persName><forename type="first">Matthew</forename><surname>Stern</surname><roleName type="degree">MD</roleName></persName><affiliation>University of Pennsylvania Health Systems, Pennsylvania Hospital, Department of Neurology, Philadelphia, Pennsylvania, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-05"></date><biblScope unit="vol">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1015">1015</biblScope><biblScope unit="page" to="1021">1021</biblScope></imprint></monogr><idno type="istex">D3143478950ED27D311D670FCE4BA2216869276B</idno><idno type="DOI">10.1002/mds.23669</idno><idno type="ArticleID">MDS23669</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>α‐synuclein</term></item><item><term>Lewy bodies</term></item><item><term>neuropathology</term></item><item><term>preclinical Parkinson's disease</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Review</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-10-12">Received</change><change when="2011-01-11">Registration</change><change when="2011-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D3143478950ED27D311D670FCE4BA2216869276B/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="60"><doi origin="wiley" registered="yes">10.1002/mds.v26.6</doi><titleGroup><title type="specialIssueTitle">25th Anniversary</title></titleGroup><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="2011-05">May 2011</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="100" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23669</doi><idGroup><id type="unit" value="MDS23669"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Review</title><title type="tocHeading1">Reviews</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-10-12"></event><event type="manuscriptRevised" date="2010-12-31"></event><event type="manuscriptAccepted" date="2011-01-11"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2012-01-27"></event><event type="publishedOnlineFinalForm" date="2011-05-27"></event><event type="firstOnline" date="2011-05-27"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1015</numbering><numbering type="pageLast">1021</numbering></numberingGroup><correspondenceTo>University College London, Reta Lila Weston Institute of Neurological Studies, 1 Wakefield Street, London WC1N 1PJ, UK</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23669.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="87"></count><count type="wordTotal" number="6052"></count></countGroup><titleGroup><title type="main" xml:lang="en">Milestones in Parkinson's disease—Clinical and pathologic features<link href="#fn1"></link></title><title type="short" xml:lang="en">Milestones in Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Glenda</givenNames><familyName>Halliday</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2" corresponding="yes"><personName><givenNames>Andrew</givenNames><familyName>Lees</familyName><degrees>MD, FRCP</degrees></personName><contactDetails><email>alees@ion.ucl.ac.uk</email></contactDetails></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Matthew</givenNames><familyName>Stern</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="AU" type="organization"><unparsedAffiliation>Neuroscience Research Australia and the University of New South Wales, Sydney, Australia</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>University College London, Reta Lila Weston Institute of Neurological Studies, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>University of Pennsylvania Health Systems, Pennsylvania Hospital, Department of Neurology, Philadelphia, Pennsylvania, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">α‐synuclein</keyword><keyword xml:id="kwd2">Lewy bodies</keyword><keyword xml:id="kwd3">neuropathology</keyword><keyword xml:id="kwd4">preclinical Parkinson's disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Glenda Halliday is a Senior Principal Research Fellowship of the National Health and Medical Research Council of Australia (fellowship #350827). Andrew Lees receives funding from the Weston Trust and the PSP (Europe) Association. Matthew Stern is a consultant to Teva, Medtronic, Ipsen, Schering‐Plough, Adamas, and Novartis.</p><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Milestones in Parkinson's disease—Clinical and pathologic features</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Milestones in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Milestones in Parkinson's disease—Clinical and pathologic features</title></titleInfo><name type="personal"><namePart type="given">Glenda</namePart><namePart type="family">Halliday</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neuroscience Research Australia and the University of New South Wales, Sydney, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew</namePart><namePart type="family">Lees</namePart><namePart type="termsOfAddress">MD, FRCP</namePart><affiliation>University College London, Reta Lila Weston Institute of Neurological Studies, London, United Kingdom</affiliation><description>Correspondence: University College London, Reta Lila Weston Institute of Neurological Studies, 1 Wakefield Street, London WC1N 1PJ, UK</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matthew</namePart><namePart type="family">Stern</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Pennsylvania Health Systems, Pennsylvania Hospital, Department of Neurology, Philadelphia, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">reviewArticle</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-05</dateIssued><dateCaptured encoding="w3cdtf">2010-10-12</dateCaptured><dateValid encoding="w3cdtf">2011-01-11</dateValid><copyrightDate encoding="w3cdtf">2011</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="references">87</extent><extent unit="words">6052</extent></physicalDescription><abstract lang="en">The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Glenda Halliday is a Senior Principal Research Fellowship of the National Health and Medical Research Council of Australia (fellowship #350827). Andrew Lees receives funding from the Weston Trust and the PSP (Europe) Association. Matthew Stern is a consultant to Teva, Medtronic, Ipsen, Schering‐Plough, Adamas, and Novartis. Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>α‐synuclein</topic><topic>Lewy bodies</topic><topic>neuropathology</topic><topic>preclinical Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Review</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2011</date><detail type="title"><title>25th Anniversary</title></detail><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1015</start><end>1021</end><total>7</total></extent></part></relatedItem><identifier type="istex">D3143478950ED27D311D670FCE4BA2216869276B</identifier><identifier type="DOI">10.1002/mds.23669</identifier><identifier type="ArticleID">MDS23669</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000565 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000565 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:D3143478950ED27D311D670FCE4BA2216869276B
|texte= Milestones in Parkinson's disease—Clinical and pathologic features
}}
| This area was generated with Dilib version V0.6.23. |  |