Milestones in PD genetics
Identifieur interne : 000A85 ( Main/Corpus ); précédent : 000A84; suivant : 000A86Milestones in PD genetics
Auteurs : Thomas Gasser ; John Hardy ; Yoshikuni MizunoSource :
- Movement Disorders [ 0885-3185 ] ; 2011-05.
English descriptors
Abstract
Over the last 25 years, genetic findings have profoundly changed our views on the etiology of Parkinson's disease. Linkage studies and positional cloning strategies have identified mutations in a number of genes that cause several monogenic autosomal‐dominant or autosomal‐recessive forms of the disorder. Although most of these Mendelian forms of Parkinson's disease are rare, whole‐genome association studies have more recently provided convincing evidence that low‐penetrance variants in at least some of these, but also in several other genes, play a direct role in the etiology of the common sporadic disease as well. In addition, rare variants with intermediate‐effect strengths in genes such as Gaucher's disease–associated glucocerebrosidase A have been discovered as important risk factors. “Next‐generation” sequencing technologies are expected by some to identify many more of these variants. Thus, an increasingly complex network of genes contributing in different ways to disease risk and progression is emerging. These findings may provide the “genetic entry points” to identify molecular targets and readouts necessary to design rational disease‐modifying treatments. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23637
Links to Exploration step
ISTEX:EA1AE26B605692ED8A62A870C498CCCE21E9F244Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Milestones in PD genetics</title><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name><affiliation><mods:affiliation>Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hardy, John" sort="Hardy, John" uniqKey="Hardy J" first="John" last="Hardy">John Hardy</name><affiliation><mods:affiliation>Reta Lilla Weston Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Mizuno, Yoshikuni" sort="Mizuno, Yoshikuni" uniqKey="Mizuno Y" first="Yoshikuni" last="Mizuno">Yoshikuni Mizuno</name><affiliation><mods:affiliation>Department of Neuro‐regenerative Medicine, Kitasato University School of Medicine, Kanagawa, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:EA1AE26B605692ED8A62A870C498CCCE21E9F244</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23637</idno><idno type="url">https://api.istex.fr/document/EA1AE26B605692ED8A62A870C498CCCE21E9F244/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000A85</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Milestones in PD genetics</title><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name><affiliation><mods:affiliation>Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hardy, John" sort="Hardy, John" uniqKey="Hardy J" first="John" last="Hardy">John Hardy</name><affiliation><mods:affiliation>Reta Lilla Weston Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Mizuno, Yoshikuni" sort="Mizuno, Yoshikuni" uniqKey="Mizuno Y" first="Yoshikuni" last="Mizuno">Yoshikuni Mizuno</name><affiliation><mods:affiliation>Department of Neuro‐regenerative Medicine, Kitasato University School of Medicine, Kanagawa, Japan</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="volume">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1042">1042</biblScope><biblScope unit="page" to="1048">1048</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">EA1AE26B605692ED8A62A870C498CCCE21E9F244</idno><idno type="DOI">10.1002/mds.23637</idno><idno type="ArticleID">MDS23637</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DNA polymorphisms</term><term>Parkinson's disease</term><term>genetic risk factors</term><term>genetics</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Over the last 25 years, genetic findings have profoundly changed our views on the etiology of Parkinson's disease. Linkage studies and positional cloning strategies have identified mutations in a number of genes that cause several monogenic autosomal‐dominant or autosomal‐recessive forms of the disorder. Although most of these Mendelian forms of Parkinson's disease are rare, whole‐genome association studies have more recently provided convincing evidence that low‐penetrance variants in at least some of these, but also in several other genes, play a direct role in the etiology of the common sporadic disease as well. In addition, rare variants with intermediate‐effect strengths in genes such as Gaucher's disease–associated glucocerebrosidase A have been discovered as important risk factors. “Next‐generation” sequencing technologies are expected by some to identify many more of these variants. Thus, an increasingly complex network of genes contributing in different ways to disease risk and progression is emerging. These findings may provide the “genetic entry points” to identify molecular targets and readouts necessary to design rational disease‐modifying treatments. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Thomas Gasser MD</name><affiliations><json:string>Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany</json:string></affiliations></json:item><json:item><name>John Hardy PhD</name><affiliations><json:string>Reta Lilla Weston Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Yoshikuni Mizuno MD</name><affiliations><json:string>Department of Neuro‐regenerative Medicine, Kitasato University School of Medicine, Kanagawa, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genetics</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genetic risk factors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>DNA polymorphisms</value></json:item></subject><articleId><json:string>MDS23637</json:string></articleId><language><json:string>eng</json:string></language><abstract>Over the last 25 years, genetic findings have profoundly changed our views on the etiology of Parkinson's disease. Linkage studies and positional cloning strategies have identified mutations in a number of genes that cause several monogenic autosomal‐dominant or autosomal‐recessive forms of the disorder. Although most of these Mendelian forms of Parkinson's disease are rare, whole‐genome association studies have more recently provided convincing evidence that low‐penetrance variants in at least some of these, but also in several other genes, play a direct role in the etiology of the common sporadic disease as well. In addition, rare variants with intermediate‐effect strengths in genes such as Gaucher's disease–associated glucocerebrosidase A have been discovered as important risk factors. “Next‐generation” sequencing technologies are expected by some to identify many more of these variants. Thus, an increasingly complex network of genes contributing in different ways to disease risk and progression is emerging. These findings may provide the “genetic entry points” to identify molecular targets and readouts necessary to design rational disease‐modifying treatments. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.052</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1215</abstractCharCount><pdfWordCount>5007</pdfWordCount><pdfCharCount>33181</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>171</abstractWordCount></qualityIndicators><title>Milestones in PD genetics</title><genre><json:string>review-article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>7</total><last>1048</last><first>1042</first></pages><issn><json:string>0885-3185</json:string></issn><issue>6</issue><subject><json:item><value>Review</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><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.23637</json:string></doi><id>EA1AE26B605692ED8A62A870C498CCCE21E9F244</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/EA1AE26B605692ED8A62A870C498CCCE21E9F244/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/EA1AE26B605692ED8A62A870C498CCCE21E9F244/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/EA1AE26B605692ED8A62A870C498CCCE21E9F244/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Milestones in PD genetics</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Relevant conflict of interest/financial disclosures: Nothing to report. 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 PD genetics</title><author><persName><forename type="first">Thomas</forename><surname>Gasser</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Hoppe‐Seyler‐Str. 3, 72076 Tübingen, Germany</p></note><affiliation>Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany</affiliation></author><author><persName><forename type="first">John</forename><surname>Hardy</surname></persName><roleName type="degree">PhD</roleName><affiliation>Reta Lilla Weston Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom</affiliation></author><author><persName><forename type="first">Yoshikuni</forename><surname>Mizuno</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neuro‐regenerative Medicine, Kitasato University School of Medicine, Kanagawa, Japan</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="volume">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1042">1042</biblScope><biblScope unit="page" to="1048">1048</biblScope></imprint></monogr><idno type="istex">EA1AE26B605692ED8A62A870C498CCCE21E9F244</idno><idno type="DOI">10.1002/mds.23637</idno><idno type="ArticleID">MDS23637</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Over the last 25 years, genetic findings have profoundly changed our views on the etiology of Parkinson's disease. Linkage studies and positional cloning strategies have identified mutations in a number of genes that cause several monogenic autosomal‐dominant or autosomal‐recessive forms of the disorder. Although most of these Mendelian forms of Parkinson's disease are rare, whole‐genome association studies have more recently provided convincing evidence that low‐penetrance variants in at least some of these, but also in several other genes, play a direct role in the etiology of the common sporadic disease as well. In addition, rare variants with intermediate‐effect strengths in genes such as Gaucher's disease–associated glucocerebrosidase A have been discovered as important risk factors. “Next‐generation” sequencing technologies are expected by some to identify many more of these variants. Thus, an increasingly complex network of genes contributing in different ways to disease risk and progression is emerging. These findings may provide the “genetic entry points” to identify molecular targets and readouts necessary to design rational disease‐modifying treatments. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>genetics</term></item><item><term>genetic risk factors</term></item><item><term>DNA polymorphisms</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="2010-12-01">Received</change><change when="2010-12-21">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/EA1AE26B605692ED8A62A870C498CCCE21E9F244/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="130" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23637</doi><idGroup><id type="unit" value="MDS23637"></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="2010-12-01"></event><event type="manuscriptAccepted" date="2010-12-21"></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">1042</numbering><numbering type="pageLast">1048</numbering></numberingGroup><correspondenceTo>Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Hoppe‐Seyler‐Str. 3, 72076 Tübingen, Germany</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23637.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="87"></count><count type="wordTotal" number="6516"></count></countGroup><titleGroup><title type="main" xml:lang="en">Milestones in PD genetics<link href="#fn21"></link></title><title type="short" xml:lang="en">Milestones in PD Genetics</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Thomas</givenNames><familyName>Gasser</familyName><degrees>MD</degrees></personName><contactDetails><email normalForm="Thomas.Gasser@uni-tuebingen.de">Thomas.Gasser@uni‐tuebingen.de</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>John</givenNames><familyName>Hardy</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Yoshikuni</givenNames><familyName>Mizuno</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Reta Lilla Weston Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neuro‐regenerative Medicine, Kitasato University School of Medicine, Kanagawa, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">genetics</keyword><keyword xml:id="kwd3">genetic risk factors</keyword><keyword xml:id="kwd4">DNA polymorphisms</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Over the last 25 years, genetic findings have profoundly changed our views on the etiology of Parkinson's disease. Linkage studies and positional cloning strategies have identified mutations in a number of genes that cause several monogenic autosomal‐dominant or autosomal‐recessive forms of the disorder. Although most of these Mendelian forms of Parkinson's disease are rare, whole‐genome association studies have more recently provided convincing evidence that low‐penetrance variants in at least some of these, but also in several other genes, play a direct role in the etiology of the common sporadic disease as well. In addition, rare variants with intermediate‐effect strengths in genes such as Gaucher's disease–associated glucocerebrosidase A have been discovered as important risk factors. “Next‐generation” sequencing technologies are expected by some to identify many more of these variants. Thus, an increasingly complex network of genes contributing in different ways to disease risk and progression is emerging. These findings may provide the “genetic entry points” to identify molecular targets and readouts necessary to design rational disease‐modifying treatments. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn21"><p><b>Relevant conflict of interest/financial disclosures:</b> Nothing to report.</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><mods version="3.6"><titleInfo lang="en"><title>Milestones in PD genetics</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Milestones in PD Genetics</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Milestones in PD genetics</title></titleInfo><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Gasser</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany</affiliation><description>Correspondence: Hertie‐Institute for Clinical Brain Research, Department of Neurodegenerative Diseases and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Hoppe‐Seyler‐Str. 3, 72076 Tübingen, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John</namePart><namePart type="family">Hardy</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Reta Lilla Weston Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshikuni</namePart><namePart type="family">Mizuno</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuro‐regenerative Medicine, Kitasato University School of Medicine, Kanagawa, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="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">2010-12-01</dateCaptured><dateValid encoding="w3cdtf">2010-12-21</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">2</extent><extent unit="tables">2</extent><extent unit="references">87</extent><extent unit="words">6516</extent></physicalDescription><abstract lang="en">Over the last 25 years, genetic findings have profoundly changed our views on the etiology of Parkinson's disease. Linkage studies and positional cloning strategies have identified mutations in a number of genes that cause several monogenic autosomal‐dominant or autosomal‐recessive forms of the disorder. Although most of these Mendelian forms of Parkinson's disease are rare, whole‐genome association studies have more recently provided convincing evidence that low‐penetrance variants in at least some of these, but also in several other genes, play a direct role in the etiology of the common sporadic disease as well. In addition, rare variants with intermediate‐effect strengths in genes such as Gaucher's disease–associated glucocerebrosidase A have been discovered as important risk factors. “Next‐generation” sequencing technologies are expected by some to identify many more of these variants. Thus, an increasingly complex network of genes contributing in different ways to disease risk and progression is emerging. These findings may provide the “genetic entry points” to identify molecular targets and readouts necessary to design rational disease‐modifying treatments. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflict of interest/financial disclosures: Nothing to report. Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>genetics</topic><topic>genetic risk factors</topic><topic>DNA polymorphisms</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><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>1042</start><end>1048</end><total>7</total></extent></part></relatedItem><identifier type="istex">EA1AE26B605692ED8A62A870C498CCCE21E9F244</identifier><identifier type="DOI">10.1002/mds.23637</identifier><identifier type="ArticleID">MDS23637</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</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)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000A85 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000A85 | 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:EA1AE26B605692ED8A62A870C498CCCE21E9F244
|texte= Milestones in PD genetics
}}
| This area was generated with Dilib version V0.6.23. |  |