Role of LINGO1 polymorphisms in Parkinson's disease.
Identifieur interne : 001A96 ( PubMed/Curation ); précédent : 001A95; suivant : 001A97Role of LINGO1 polymorphisms in Parkinson's disease.
Auteurs : Dietrich Haubenberger [Autriche] ; Christoph Hotzy ; Walter Pirker ; Regina Katzenschlager ; Thomas Brücke ; Fritz Zimprich ; Eduard Auff ; Alexander ZimprichSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
Descripteurs français
- Wicri :
- geographic : Autriche.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Membrane Proteins, Nerve Tissue Proteins.
- geographic : Austria.
- genetics : Parkinson Disease, Polymorphism, Single Nucleotide.
- Aged, Female, Gene Frequency, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged.
Abstract
A clinical overlap between Parkinson's disease (PD) and essential tremor (ET) has prompted a discussion whether these conditions share common genetic susceptibility factors. Recently, the first genome-wide association study in ET revealed a significant association with a variant in the LINGO1 gene. LINGO1 has also been demonstrated to play a role in the survival of dopaminergic neurons in an animal model of PD, and therefore constitutes a potential candidate gene for PD. In this study, SNPs rs9652490, rs11856808, and rs7177008 of LINGO1 were genotyped in a total of 694 Austrian subjects (349 PD, 345 controls). No association could be found between genotype or allele counts and PD. Neither did a subgroup analysis in tremor-dominant patients with PD reveal a significant association. This study on LINGO1-variants in PD argues against a major role of LINGO1 gene variations for PD.
DOI: 10.1002/mds.22768
PubMed: 19908305
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uniqKey="Katzenschlager R" first="Regina" last="Katzenschlager">Regina Katzenschlager</name></author><author><name sortKey="Brucke, Thomas" sort="Brucke, Thomas" uniqKey="Brucke T" first="Thomas" last="Brücke">Thomas Brücke</name></author><author><name sortKey="Zimprich, Fritz" sort="Zimprich, Fritz" uniqKey="Zimprich F" first="Fritz" last="Zimprich">Fritz Zimprich</name></author><author><name sortKey="Auff, Eduard" sort="Auff, Eduard" uniqKey="Auff E" first="Eduard" last="Auff">Eduard Auff</name></author><author><name sortKey="Zimprich, Alexander" sort="Zimprich, Alexander" uniqKey="Zimprich A" first="Alexander" last="Zimprich">Alexander Zimprich</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="doi">10.1002/mds.22768</idno><idno type="RBID">pubmed:19908305</idno><idno type="pmid">19908305</idno><idno type="wicri:Area/PubMed/Corpus">001A96</idno><idno 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xml:lang="en"><term>Aged</term><term>Female</term><term>Gene Frequency</term><term>Genome-Wide Association Study</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="Wicri" type="geographic" xml:lang="fr"><term>Autriche</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A clinical overlap between Parkinson's disease (PD) and essential tremor (ET) has prompted a discussion whether these conditions share common genetic susceptibility factors. Recently, the first genome-wide association study in ET revealed a significant association with a variant in the LINGO1 gene. LINGO1 has also been demonstrated to play a role in the survival of dopaminergic neurons in an animal model of PD, and therefore constitutes a potential candidate gene for PD. In this study, SNPs rs9652490, rs11856808, and rs7177008 of LINGO1 were genotyped in a total of 694 Austrian subjects (349 PD, 345 controls). No association could be found between genotype or allele counts and PD. Neither did a subgroup analysis in tremor-dominant patients with PD reveal a significant association. This study on LINGO1-variants in PD argues against a major role of LINGO1 gene variations for PD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">19908305</PMID><DateCreated><Year>2009</Year><Month>12</Month><Day>28</Day></DateCreated><DateCompleted><Year>2010</Year><Month>03</Month><Day>04</Day></DateCompleted><DateRevised><Year>2015</Year><Month>03</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>16</Issue><PubDate><Year>2009</Year><Month>Dec</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Role of LINGO1 polymorphisms in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>2404-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22768</ELocationID><Abstract><AbstractText>A clinical overlap between Parkinson's disease (PD) and essential tremor (ET) has prompted a discussion whether these conditions share common genetic susceptibility factors. Recently, the first genome-wide association study in ET revealed a significant association with a variant in the LINGO1 gene. LINGO1 has also been demonstrated to play a role in the survival of dopaminergic neurons in an animal model of PD, and therefore constitutes a potential candidate gene for PD. In this study, SNPs rs9652490, rs11856808, and rs7177008 of LINGO1 were genotyped in a total of 694 Austrian subjects (349 PD, 345 controls). No association could be found between genotype or allele counts and PD. Neither did a subgroup analysis in tremor-dominant patients with PD reveal a significant association. This study on LINGO1-variants in PD argues against a major role of LINGO1 gene variations for PD.</AbstractText><CopyrightInformation>(c) 2009 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Haubenberger</LastName><ForeName>Dietrich</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Neurology, Medical University of Vienna, Vienna, Austria. dietrich.haubenberger@meduniwien.ac.at</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hotzy</LastName><ForeName>Christoph</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Pirker</LastName><ForeName>Walter</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Katzenschlager</LastName><ForeName>Regina</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Brücke</LastName><ForeName>Thomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Zimprich</LastName><ForeName>Fritz</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Auff</LastName><ForeName>Eduard</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Zimprich</LastName><ForeName>Alexander</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>Z99 NS999999</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C482293">LINGO1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2006 Mar;63(3):354-7</RefSource><PMID Version="1">16533962</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1991 Feb;41(2 ( Pt 1)):234-8</RefSource><PMID Version="1">1992367</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2007 Dec;130(Pt 12):3297-307</RefSource><PMID Version="1">18025031</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2008 Apr 15;70(16 Pt 2):1452-5</RefSource><PMID Version="1">18413570</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2008 May 15;23(7):993-7</RefSource><PMID Version="1">18383536</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 2009 Mar;41(3):277-9</RefSource><PMID Version="1">19182806</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Neurosurg Psychiatry. 2009 Apr;80(4):423-5</RefSource><PMID Version="1">19289477</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2004 Aug;10(6):357-62</RefSource><PMID Version="1">15261877</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2004 Mar;7(3):221-8</RefSource><PMID Version="1">14966521</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2007 Mar 15;22(4):559-63</RefSource><PMID Version="1">17149727</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2007 Aug 15;22(11):1607-14</RefSource><PMID Version="1">17546668</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2007 Sep 4;104(36):14430-5</RefSource><PMID Version="1">17726113</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1988 Jul;24(1):23-6</RefSource><PMID Version="1">3415197</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1994 Jun;35(6):717-23</RefSource><PMID Version="1">8210229</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2006 Oct 23;407(2):97-100</RefSource><PMID Version="1">16939701</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" Type="Geographic" UI="D001317">Austria</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" 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