LINGO1 is not associated with Parkinson's disease in German patients
Identifieur interne : 001088 ( Main/Corpus ); précédent : 001087; suivant : 001089LINGO1 is not associated with Parkinson's disease in German patients
Auteurs : Stephan Klebe ; Sandra Thier ; Delia Lorenz ; Michael Nothnagel ; Stefan Schreiber ; Christine Klein ; Johann Hagenah ; Meike Kasten ; Daniela Berg ; Karin Srulijes ; Thomas Gasser ; Günther Deuschl ; Gregor Kuhlenb UmerSource :
- American Journal of Medical Genetics Part B: Neuropsychiatric Genetics [ 1552-4841 ] ; 2010-09.
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Abstract
Essential tremor (ET) and Parkinson's disease (PD) are the most common movement disorders and show clinical, genetic, and pathophysiological overlap. Single‐nucleotide polymorphisms (SNPs) in the leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein gene (LINGO1) are associated with ET. LINGO1 is overexpressed in the substantia nigra (SN) of PD patients and inhibition of LINGO1 confers neuroprotection in a rodent model of PD. In this study we test the hypothesis whether SNPs in the LINGO1 gene that are associated with ET are also associated with PD. Three large German case–control samples from Kiel, Lübeck, and Tübingen (total: 1,798 cases and 1,482 controls) were genotyped for the three LINGO1 SNPs associated with ET. Association was assessed using allele‐ and genotype‐based tests in each of the three samples separately, in the combined sample, and in subsets of patients with early‐onset PD (<50 years) and of patients with a positive family history of PD. Neither of the three samples alone nor the combined sample showed evidence for association between LINGO1 SNPs and PD. The allele‐based test showed a trend toward nominal association for all three SNPs in the Kiel sample. The subsets with early‐onset PD or a positive family history did also not reveal evidence for association. SNPs in the LINGO1 gene associated with ET could not be shown to be associated with PD in our study population, despite a postulated overlap between both diseases. © 2010 Wiley‐Liss, Inc.
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DOI: 10.1002/ajmg.b.31085
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last="Thier">Sandra Thier</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lorenz, Delia" sort="Lorenz, Delia" uniqKey="Lorenz D" first="Delia" last="Lorenz">Delia Lorenz</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Nothnagel, Michael" sort="Nothnagel, Michael" uniqKey="Nothnagel M" first="Michael" last="Nothnagel">Michael Nothnagel</name><affiliation><mods:affiliation>Institute of Medical Informatics and Statistics, Christian‐Albrechts University, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schreiber, Stefan" sort="Schreiber, Stefan" uniqKey="Schreiber S" first="Stefan" last="Schreiber">Stefan Schreiber</name><affiliation><mods:affiliation>Institute of Clinical Molecular Biology, Christian‐Albrechts University, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><mods:affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hagenah, Johann" sort="Hagenah, Johann" uniqKey="Hagenah J" first="Johann" last="Hagenah">Johann Hagenah</name><affiliation><mods:affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kasten, Meike" sort="Kasten, Meike" uniqKey="Kasten M" first="Meike" last="Kasten">Meike Kasten</name><affiliation><mods:affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Berg, Daniela" sort="Berg, Daniela" uniqKey="Berg D" first="Daniela" last="Berg">Daniela Berg</name><affiliation><mods:affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Srulijes, Karin" sort="Srulijes, Karin" uniqKey="Srulijes K" first="Karin" last="Srulijes">Karin Srulijes</name><affiliation><mods:affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</mods:affiliation></affiliation></author><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, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Deuschl, Gunther" sort="Deuschl, Gunther" uniqKey="Deuschl G" first="Günther" last="Deuschl">Günther Deuschl</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kuhlenb Umer, Gregor" sort="Kuhlenb Umer, Gregor" uniqKey="Kuhlenb Umer G" first="Gregor" last="Kuhlenb Umer">Gregor Kuhlenb Umer</name><affiliation><mods:affiliation>Institute of Experimental Medicine, Christian‐Albrechts University, Kiel, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title><title level="j" type="abbrev">Am. 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Genet.</title><idno type="ISSN">1552-4841</idno><idno type="eISSN">1552-485X</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-09">2010-09</date><biblScope unit="volume">153B</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1173">1173</biblScope><biblScope unit="page" to="1178">1178</biblScope></imprint><idno type="ISSN">1552-4841</idno></series><idno type="istex">AF4E972DA4E896A7D520B00D3E22B9051BA5E692</idno><idno type="DOI">10.1002/ajmg.b.31085</idno><idno type="ArticleID">AJMG31085</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1552-4841</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>LINGO1</term><term>Parkinson disease</term><term>association study</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="de">Essential tremor (ET) and Parkinson's disease (PD) are the most common movement disorders and show clinical, genetic, and pathophysiological overlap. Single‐nucleotide polymorphisms (SNPs) in the leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein gene (LINGO1) are associated with ET. LINGO1 is overexpressed in the substantia nigra (SN) of PD patients and inhibition of LINGO1 confers neuroprotection in a rodent model of PD. In this study we test the hypothesis whether SNPs in the LINGO1 gene that are associated with ET are also associated with PD. Three large German case–control samples from Kiel, Lübeck, and Tübingen (total: 1,798 cases and 1,482 controls) were genotyped for the three LINGO1 SNPs associated with ET. Association was assessed using allele‐ and genotype‐based tests in each of the three samples separately, in the combined sample, and in subsets of patients with early‐onset PD (<50 years) and of patients with a positive family history of PD. Neither of the three samples alone nor the combined sample showed evidence for association between LINGO1 SNPs and PD. The allele‐based test showed a trend toward nominal association for all three SNPs in the Kiel sample. The subsets with early‐onset PD or a positive family history did also not reveal evidence for association. SNPs in the LINGO1 gene associated with ET could not be shown to be associated with PD in our study population, despite a postulated overlap between both diseases. © 2010 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Stephan Klebe</name><affiliations><json:string>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Sandra Thier</name><affiliations><json:string>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Delia Lorenz</name><affiliations><json:string>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Michael Nothnagel</name><affiliations><json:string>Institute of Medical Informatics and Statistics, Christian‐Albrechts University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Stefan Schreiber</name><affiliations><json:string>Institute of Clinical Molecular Biology, Christian‐Albrechts University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Christine Klein</name><affiliations><json:string>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Johann Hagenah</name><affiliations><json:string>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Meike Kasten</name><affiliations><json:string>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Daniela Berg</name><affiliations><json:string>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Karin Srulijes</name><affiliations><json:string>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Thomas Gasser</name><affiliations><json:string>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Günther Deuschl</name><affiliations><json:string>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Gregor Kuhlenbäumer</name><affiliations><json:string>Institute of Experimental Medicine, Christian‐Albrechts University, Kiel, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>LINGO1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>association study</value></json:item></subject><articleId><json:string>AJMG31085</json:string></articleId><language><json:string>eng</json:string></language><abstract>Essential tremor (ET) and Parkinson's disease (PD) are the most common movement disorders and show clinical, genetic, and pathophysiological overlap. Single‐nucleotide polymorphisms (SNPs) in the leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein gene (LINGO1) are associated with ET. LINGO1 is overexpressed in the substantia nigra (SN) of PD patients and inhibition of LINGO1 confers neuroprotection in a rodent model of PD. In this study we test the hypothesis whether SNPs in the LINGO1 gene that are associated with ET are also associated with PD. Three large German case–control samples from Kiel, Lübeck, and Tübingen (total: 1,798 cases and 1,482 controls) were genotyped for the three LINGO1 SNPs associated with ET. Association was assessed using allele‐ and genotype‐based tests in each of the three samples separately, in the combined sample, and in subsets of patients with early‐onset PD (>50 years) and of patients with a positive family history of PD. Neither of the three samples alone nor the combined sample showed evidence for association between LINGO1 SNPs and PD. The allele‐based test showed a trend toward nominal association for all three SNPs in the Kiel sample. The subsets with early‐onset PD or a positive family history did also not reveal evidence for association. SNPs in the LINGO1 gene associated with ET could not be shown to be associated with PD in our study population, despite a postulated overlap between both diseases. © 2010 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>6.532</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1536</abstractCharCount><pdfWordCount>3688</pdfWordCount><pdfCharCount>23842</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>237</abstractWordCount></qualityIndicators><title>LINGO1 is not associated with Parkinson's disease in German patients</title><genre><json:string>article</json:string></genre><host><volume>153B</volume><publisherId><json:string>AJMG</json:string></publisherId><pages><total>6</total><last>1178</last><first>1173</first></pages><issn><json:string>1552-4841</json:string></issn><issue>6</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1552-485X</json:string></eissn><title>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title><doi><json:string>10.1002/(ISSN)1552-485X</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/ajmg.b.31085</json:string></doi><id>AF4E972DA4E896A7D520B00D3E22B9051BA5E692</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/AF4E972DA4E896A7D520B00D3E22B9051BA5E692/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/AF4E972DA4E896A7D520B00D3E22B9051BA5E692/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/AF4E972DA4E896A7D520B00D3E22B9051BA5E692/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">LINGO1 is not associated with Parkinson's disease in German patients</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*How to Cite this Article: Klebe S, Thier S, Lorenz D, Nothnagel M, Schreiber S, Klein C, Hagenah J, Kasten M, Berg D, Srulijes K, Gasser T, Deuschl G, Kuhlenbäumer G. 2010. LINGO1 Is Not Associated With Parkinson's Disease in German Patients. Am J Med Genet Part B 153B:1173–1178.</note><note type="content">*Stephan Klebe, Sandra Thier, Günther Deuschl, and Gregor Kuhlenbäumer contributed equally to this work.</note><note>German Federal Ministry of Education and Research - No. 01GI0201;</note><note>Medical Faculty of the Kiel University</note><note>Cluster of Excellence “Inflammation at Interfaces”</note><note>Christian‐Albrechts University, Kiel</note><note>Ministry for Science, Commerce and Transportation of Schleswig‐Holstein, Germany</note><note>German National Genome Research Network (NGFN, POPGEN Biobank) - No. BMBF 01GR0468; No. BMBF 01GS0809;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">LINGO1 is not associated with Parkinson's disease in German patients</title><author><persName><forename type="first">Stephan</forename><surname>Klebe</surname></persName><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation></author><author><persName><forename type="first">Sandra</forename><surname>Thier</surname></persName><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation></author><author><persName><forename type="first">Delia</forename><surname>Lorenz</surname></persName><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation></author><author><persName><forename type="first">Michael</forename><surname>Nothnagel</surname></persName><affiliation>Institute of Medical Informatics and Statistics, Christian‐Albrechts University, Kiel, Germany</affiliation></author><author><persName><forename type="first">Stefan</forename><surname>Schreiber</surname></persName><affiliation>Institute of Clinical Molecular Biology, Christian‐Albrechts University, Kiel, Germany</affiliation></author><author><persName><forename type="first">Christine</forename><surname>Klein</surname></persName><affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Johann</forename><surname>Hagenah</surname></persName><affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Meike</forename><surname>Kasten</surname></persName><affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Daniela</forename><surname>Berg</surname></persName><affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Karin</forename><surname>Srulijes</surname></persName><affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Thomas</forename><surname>Gasser</surname></persName><affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Günther</forename><surname>Deuschl</surname></persName><note type="correspondence"><p>Correspondence: Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Arnold‐Heller Str. 3, D‐24105 Kiel, Germany.</p></note><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation></author><author><persName><forename type="first">Gregor</forename><surname>Kuhlenbäumer</surname></persName><affiliation>Institute of Experimental Medicine, Christian‐Albrechts University, Kiel, Germany</affiliation></author></analytic><monogr><title level="j">American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title><title level="j" type="abbrev">Am. J. Med. Genet.</title><idno type="pISSN">1552-4841</idno><idno type="eISSN">1552-485X</idno><idno type="DOI">10.1002/(ISSN)1552-485X</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-09"></date><biblScope unit="volume">153B</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1173">1173</biblScope><biblScope unit="page" to="1178">1178</biblScope></imprint></monogr><idno type="istex">AF4E972DA4E896A7D520B00D3E22B9051BA5E692</idno><idno type="DOI">10.1002/ajmg.b.31085</idno><idno type="ArticleID">AJMG31085</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="de"><p>Essential tremor (ET) and Parkinson's disease (PD) are the most common movement disorders and show clinical, genetic, and pathophysiological overlap. Single‐nucleotide polymorphisms (SNPs) in the leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein gene (LINGO1) are associated with ET. LINGO1 is overexpressed in the substantia nigra (SN) of PD patients and inhibition of LINGO1 confers neuroprotection in a rodent model of PD. In this study we test the hypothesis whether SNPs in the LINGO1 gene that are associated with ET are also associated with PD. Three large German case–control samples from Kiel, Lübeck, and Tübingen (total: 1,798 cases and 1,482 controls) were genotyped for the three LINGO1 SNPs associated with ET. Association was assessed using allele‐ and genotype‐based tests in each of the three samples separately, in the combined sample, and in subsets of patients with early‐onset PD (<50 years) and of patients with a positive family history of PD. Neither of the three samples alone nor the combined sample showed evidence for association between LINGO1 SNPs and PD. The allele‐based test showed a trend toward nominal association for all three SNPs in the Kiel sample. The subsets with early‐onset PD or a positive family history did also not reveal evidence for association. SNPs in the LINGO1 gene associated with ET could not be shown to be associated with PD in our study population, despite a postulated overlap between both diseases. © 2010 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>LINGO1</term></item><item><term>Parkinson disease</term></item><item><term>association study</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2009-10-16">Received</change><change when="2010-02-18">Registration</change><change when="2010-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/AF4E972DA4E896A7D520B00D3E22B9051BA5E692/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)1552-485X</doi><issn type="print">1552-4841</issn><issn type="electronic">1552-485X</issn><idGroup><id type="product" value="AJMG"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="AMERICAN JOURNAL OF MEDICAL GENETICS PART B: NEUROPSYCHIATRIC GENETICS">American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title><title type="short">Am. J. Med. Genet.</title></titleGroup><selfCitationGroup><citation type="ancestor" xml:id="cit1"><journalTitle>American Journal of Medical Genetics</journalTitle><accessionId ref="info:x-wiley/issn/01487299">0148-7299</accessionId><accessionId ref="info:x-wiley/issn/10968628">1096-8628</accessionId><pubYear year="2004">2004</pubYear></citation></selfCitationGroup></publicationMeta><publicationMeta level="part" position="60"><doi origin="wiley" registered="yes">10.1002/ajmg.b.v153b:6</doi><numberingGroup><numbering type="journalVolume" number="153">153B</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="2010-09">September 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="70" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ajmg.b.31085</doi><idGroup><id type="unit" value="AJMG31085"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2010 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2009-10-16"></event><event type="manuscriptAccepted" date="2010-02-18"></event><event type="firstOnline" date="2010-04-05"></event><event type="publishedOnlineFinalForm" date="2010-08-02"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-04-05"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:FullText result:FullText" date="2011-02-24"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-02"></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">1173</numbering><numbering type="pageLast">1178</numbering></numberingGroup><correspondenceTo>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Arnold‐Heller Str. 3, D‐24105 Kiel, Germany.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:AJMG.AJMG31085.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="25"></count><count type="wordTotal" number="4914"></count></countGroup><titleGroup><title type="main" xml:lang="en"><i>LINGO1</i> is not associated with Parkinson's disease in German patients<link href="#fn1"></link> <link href="#fn2"></link></title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Stephan</givenNames><familyName>Klebe</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Sandra</givenNames><familyName>Thier</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Delia</givenNames><familyName>Lorenz</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Michael</givenNames><familyName>Nothnagel</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Stefan</givenNames><familyName>Schreiber</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Christine</givenNames><familyName>Klein</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Johann</givenNames><familyName>Hagenah</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Meike</givenNames><familyName>Kasten</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Daniela</givenNames><familyName>Berg</familyName></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Karin</givenNames><familyName>Srulijes</familyName></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Thomas</givenNames><familyName>Gasser</familyName></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Günther</givenNames><familyName>Deuschl</familyName></personName><contactDetails><email normalForm="g.deuschl@neurologie.uni-kiel.de">g.deuschl@neurologie.uni‐kiel.de</email></contactDetails></creator><creator xml:id="au13" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Gregor</givenNames><familyName>Kuhlenbäumer</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Medical Informatics and Statistics, Christian‐Albrechts University, Kiel, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Clinical Molecular Biology, Christian‐Albrechts University, Kiel, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="DE" type="organization"><unparsedAffiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Experimental Medicine, Christian‐Albrechts University, Kiel, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">LINGO1</keyword><keyword xml:id="kwd2">Parkinson disease</keyword><keyword xml:id="kwd3">association study</keyword></keywordGroup><fundingInfo><fundingAgency>German Federal Ministry of Education and Research</fundingAgency><fundingNumber>01GI0201</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Medical Faculty of the Kiel University</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Cluster of Excellence “Inflammation at Interfaces”</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Christian‐Albrechts University, Kiel</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Ministry for Science, Commerce and Transportation of Schleswig‐Holstein, Germany</fundingAgency></fundingInfo><fundingInfo><fundingAgency>German National Genome Research Network (NGFN, POPGEN Biobank)</fundingAgency><fundingNumber>BMBF 01GR0468</fundingNumber><fundingNumber>BMBF 01GS0809</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="de"><title type="main">Abstract</title><p>Essential tremor (ET) and Parkinson's disease (PD) are the most common movement disorders and show clinical, genetic, and pathophysiological overlap. Single‐nucleotide polymorphisms (SNPs) in the leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein gene (<i>LINGO1</i>) are associated with ET. <i>LINGO1</i> is overexpressed in the substantia nigra (SN) of PD patients and inhibition of LINGO1 confers neuroprotection in a rodent model of PD. In this study we test the hypothesis whether SNPs in the <i>LINGO1</i> gene that are associated with ET are also associated with PD. Three large German case–control samples from Kiel, Lübeck, and Tübingen (total: 1,798 cases and 1,482 controls) were genotyped for the three <i>LINGO1</i> SNPs associated with ET. Association was assessed using allele‐ and genotype‐based tests in each of the three samples separately, in the combined sample, and in subsets of patients with early‐onset PD (<50 years) and of patients with a positive family history of PD. Neither of the three samples alone nor the combined sample showed evidence for association between <i>LINGO1</i> SNPs and PD. The allele‐based test showed a trend toward nominal association for all three SNPs in the Kiel sample. The subsets with early‐onset PD or a positive family history did also not reveal evidence for association. SNPs in the <i>LINGO1</i> gene associated with ET could not be shown to be associated with PD in our study population, despite a postulated overlap between both diseases. © 2010 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>How to Cite this Article: Klebe S, Thier S, Lorenz D, Nothnagel M, Schreiber S, Klein C, Hagenah J, Kasten M, Berg D, Srulijes K, Gasser T, Deuschl G, Kuhlenbäumer G. 2010. <i>LINGO1</i> Is Not Associated With Parkinson's Disease in German Patients. Am J Med Genet Part B 153B:1173–1178.</p></note><note xml:id="fn2"><p>Stephan Klebe, Sandra Thier, Günther Deuschl, and Gregor Kuhlenbäumer contributed equally to this work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>LINGO1 is not associated with Parkinson's disease in German patients</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>is not associated with Parkinson's disease in German patients</title></titleInfo><name type="personal"><namePart type="given">Stephan</namePart><namePart type="family">Klebe</namePart><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sandra</namePart><namePart type="family">Thier</namePart><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Delia</namePart><namePart type="family">Lorenz</namePart><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Nothnagel</namePart><affiliation>Institute of Medical Informatics and Statistics, Christian‐Albrechts University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stefan</namePart><namePart type="family">Schreiber</namePart><affiliation>Institute of Clinical Molecular Biology, Christian‐Albrechts University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Klein</namePart><affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Johann</namePart><namePart type="family">Hagenah</namePart><affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Meike</namePart><namePart type="family">Kasten</namePart><affiliation>Section of Clinical and Molecular Neurogenetics, Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniela</namePart><namePart type="family">Berg</namePart><affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karin</namePart><namePart type="family">Srulijes</namePart><affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Gasser</namePart><affiliation>Hertie‐Institute for Clinical Brain Research, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Günther</namePart><namePart type="family">Deuschl</namePart><affiliation>Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Kiel, Germany</affiliation><description>Correspondence: Department of Neurology, University Hospital Schleswig‐Holstein, Campus Kiel, Arnold‐Heller Str. 3, D‐24105 Kiel, Germany.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregor</namePart><namePart type="family">Kuhlenbäumer</namePart><affiliation>Institute of Experimental Medicine, Christian‐Albrechts University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-09</dateIssued><dateCaptured encoding="w3cdtf">2009-10-16</dateCaptured><dateValid encoding="w3cdtf">2010-02-18</dateValid><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><extent unit="tables">3</extent><extent unit="references">25</extent><extent unit="words">4914</extent></physicalDescription><abstract lang="de">Essential tremor (ET) and Parkinson's disease (PD) are the most common movement disorders and show clinical, genetic, and pathophysiological overlap. Single‐nucleotide polymorphisms (SNPs) in the leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein gene (LINGO1) are associated with ET. LINGO1 is overexpressed in the substantia nigra (SN) of PD patients and inhibition of LINGO1 confers neuroprotection in a rodent model of PD. In this study we test the hypothesis whether SNPs in the LINGO1 gene that are associated with ET are also associated with PD. Three large German case–control samples from Kiel, Lübeck, and Tübingen (total: 1,798 cases and 1,482 controls) were genotyped for the three LINGO1 SNPs associated with ET. Association was assessed using allele‐ and genotype‐based tests in each of the three samples separately, in the combined sample, and in subsets of patients with early‐onset PD (<50 years) and of patients with a positive family history of PD. Neither of the three samples alone nor the combined sample showed evidence for association between LINGO1 SNPs and PD. The allele‐based test showed a trend toward nominal association for all three SNPs in the Kiel sample. The subsets with early‐onset PD or a positive family history did also not reveal evidence for association. SNPs in the LINGO1 gene associated with ET could not be shown to be associated with PD in our study population, despite a postulated overlap between both diseases. © 2010 Wiley‐Liss, Inc.</abstract><note type="content">*How to Cite this Article: Klebe S, Thier S, Lorenz D, Nothnagel M, Schreiber S, Klein C, Hagenah J, Kasten M, Berg D, Srulijes K, Gasser T, Deuschl G, Kuhlenbäumer G. 2010. LINGO1 Is Not Associated With Parkinson's Disease in German Patients. Am J Med Genet Part B 153B:1173–1178.</note><note type="content">*Stephan Klebe, Sandra Thier, Günther Deuschl, and Gregor Kuhlenbäumer contributed equally to this work.</note><note type="funding">German Federal Ministry of Education and Research - No. 01GI0201; </note><note type="funding">Medical Faculty of the Kiel University</note><note type="funding">Cluster of Excellence “Inflammation at Interfaces”</note><note type="funding">Christian‐Albrechts University, Kiel</note><note type="funding">Ministry for Science, Commerce and Transportation of Schleswig‐Holstein, Germany</note><note type="funding">German National Genome Research Network (NGFN, POPGEN Biobank) - No. BMBF 01GR0468; No. BMBF 01GS0809; </note><subject lang="en"><genre>Keywords</genre><topic>LINGO1</topic><topic>Parkinson disease</topic><topic>association study</topic></subject><relatedItem type="host"><titleInfo><title>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title></titleInfo><titleInfo type="abbreviated"><title>Am. J. Med. Genet.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1552-4841</identifier><identifier type="eISSN">1552-485X</identifier><identifier type="DOI">10.1002/(ISSN)1552-485X</identifier><identifier type="PublisherID">AJMG</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>153B</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1173</start><end>1178</end><total>6</total></extent></part></relatedItem><relatedItem type="preceding"><titleInfo><title>American Journal of Medical Genetics</title></titleInfo><identifier type="ISSN">0148-7299</identifier><identifier type="ISSN">1096-8628</identifier><part><date point="end">2004</date></part></relatedItem><identifier type="istex">AF4E972DA4E896A7D520B00D3E22B9051BA5E692</identifier><identifier type="DOI">10.1002/ajmg.b.31085</identifier><identifier type="ArticleID">AJMG31085</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Wiley‐Liss, Inc.</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)
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