Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease
Identifieur interne : 002744 ( Main/Corpus ); précédent : 002743; suivant : 002745Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease
Auteurs : M. Martinez ; A. Brice ; J R Vaughan ; A. Zimprich ; M M B. Breteler ; G. Meco ; A. Filla ; M J Farrer ; C. Bétard ; J. Hardy ; G. De Michele ; V. Bonifati ; B. Oostra ; T. Gasser ; N W Wood ; A. DürrSource :
- Journal of Medical Genetics [ 0022-2593 ] ; 2004-12.
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Abstract
Objective: To undertake a full genome-wide screen for Parkinson’s disease susceptibility loci. Methods: A genome-wide linkage study was undertaken in 227 affected sibling pairs from 199 pedigrees with Parkinson’s disease. The pedigree sample consisted of 188 pedigrees from five European countries, and 11 from the USA. Individuals were genotyped for 391 microsatellite markers at ∼10 cM intervals throughout the genome. Multipoint model-free affected sibling pair linkage analyses were carried out using the MLS (maximum LOD score) test. Results: There were six chromosomal regions with maximum MLS peaks of 1 or greater (pointwise p<0.018). Four of these chromosomal regions appear to be newly identified regions, and the highest MLS values were obtained on chromosomes 11q (MLS = 1.60, at 91 cM, D11S4175) and 7p (MLS = 1.51, at 5 cM, D7S531). The remaining two MLS peaks, on 2p11–q12 and 5q23, are consistent with excess sharing in regions reported by other studies. The highest MLS peak was observed on chromosome 2p11–q12 (MLS = 2.04, between markers D2S2216 and D2S160), within a relatively short distance (∼17 cM) from the PARK3 region. Although a stronger support of linkage to this region was observed in the late age of onset subgroup of families, these differences were not significant. The peak on 5q23 (MLS = 1.05, at 130 cM, D5S471) coincides with the region identified by three other genome scans. All peak locations fell within a 10 cM distance. Conclusions: These stratified linkage analyses suggest linkage heterogeneity within the sample across the 2p11–q12 and 5q23 regions, with these two regions contributing independently to Parkinson’s disease susceptibility.
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DOI: 10.1136/jmg.2004.022632
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Brice</name><affiliation><mods:affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Vaughan, J R" sort="Vaughan, J R" uniqKey="Vaughan J" first="J R" last="Vaughan">J R Vaughan</name><affiliation><mods:affiliation>Department of Neurology Charing Cross Hospital, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Zimprich, A" sort="Zimprich, A" uniqKey="Zimprich A" first="A" last="Zimprich">A. Zimprich</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Breteler, M M B" sort="Breteler, M M B" uniqKey="Breteler M" first="M M B" last="Breteler">M M B. 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Oostra</name><affiliation><mods:affiliation>Department of Clinical Genetics, Erasmus University, Rotterdam, Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Gasser, T" sort="Gasser, T" uniqKey="Gasser T" first="T" last="Gasser">T. Gasser</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wood, N W" sort="Wood, N W" uniqKey="Wood N" first="N W" last="Wood">N W Wood</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Durr, A" sort="Durr, A" uniqKey="Durr A" first="A" last="Dürr">A. Dürr</name><affiliation><mods:affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA</idno><date when="2004" year="2004">2004</date><idno type="doi">10.1136/jmg.2004.022632</idno><idno type="url">https://api.istex.fr/document/CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002744</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease</title><author><name sortKey="Martinez, M" sort="Martinez, M" uniqKey="Martinez M" first="M" last="Martinez">M. Martinez</name><affiliation><mods:affiliation>INSERM EMI00-06, Evry, France</mods:affiliation></affiliation></author><author><name sortKey="Brice, A" sort="Brice, A" uniqKey="Brice A" first="A" last="Brice">A. Brice</name><affiliation><mods:affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Vaughan, J R" sort="Vaughan, J R" uniqKey="Vaughan J" first="J R" last="Vaughan">J R Vaughan</name><affiliation><mods:affiliation>Department of Neurology Charing Cross Hospital, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Zimprich, A" sort="Zimprich, A" uniqKey="Zimprich A" first="A" last="Zimprich">A. Zimprich</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Breteler, M M B" sort="Breteler, M M B" uniqKey="Breteler M" first="M M B" last="Breteler">M M B. Breteler</name><affiliation><mods:affiliation>Department of Epidemiology and Biostatistics, Erasmus University, Rotterdam, Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Meco, G" sort="Meco, G" uniqKey="Meco G" first="G" last="Meco">G. Meco</name><affiliation><mods:affiliation>Department of Neurological Sciences, La Sapienza University, Rome, Italy</mods:affiliation></affiliation></author><author><name sortKey="Filla, A" sort="Filla, A" uniqKey="Filla A" first="A" last="Filla">A. Filla</name><affiliation><mods:affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Farrer, M J" sort="Farrer, M J" uniqKey="Farrer M" first="M J" last="Farrer">M J Farrer</name><affiliation><mods:affiliation>Neurogenetics Laboratory, Mayo Clinic Jacksonville, Florida, USA</mods:affiliation></affiliation></author><author><name sortKey="Betard, C" sort="Betard, C" uniqKey="Betard C" first="C" last="Bétard">C. Bétard</name><affiliation><mods:affiliation>Centre National de Génotypage, Evry, France</mods:affiliation></affiliation></author><author><name sortKey="Hardy, J" sort="Hardy, J" uniqKey="Hardy J" first="J" last="Hardy">J. Hardy</name><affiliation><mods:affiliation>Laboratory of Neurogenetics, National Institute on Aging, NIH, Bethesda, Maryland, USA</mods:affiliation></affiliation></author><author><name sortKey="De Michele, G" sort="De Michele, G" uniqKey="De Michele G" first="G" last="De Michele">G. De Michele</name><affiliation><mods:affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Bonifati, V" sort="Bonifati, V" uniqKey="Bonifati V" first="V" last="Bonifati">V. Bonifati</name><affiliation><mods:affiliation>Department of Neurological Sciences, La Sapienza University, Rome, Italy</mods:affiliation></affiliation></author><author><name sortKey="Oostra, B" sort="Oostra, B" uniqKey="Oostra B" first="B" last="Oostra">B. Oostra</name><affiliation><mods:affiliation>Department of Clinical Genetics, Erasmus University, Rotterdam, Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Gasser, T" sort="Gasser, T" uniqKey="Gasser T" first="T" last="Gasser">T. Gasser</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wood, N W" sort="Wood, N W" uniqKey="Wood N" first="N W" last="Wood">N W Wood</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Durr, A" sort="Durr, A" uniqKey="Durr A" first="A" last="Dürr">A. Dürr</name><affiliation><mods:affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Medical Genetics</title><title level="j" type="abbrev">J Med Genet</title><idno type="ISSN">0022-2593</idno><idno type="eISSN">1468-6244</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2004-12">2004-12</date><biblScope unit="volume">41</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="900">900</biblScope></imprint><idno type="ISSN">0022-2593</idno></series><idno type="istex">CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA</idno><idno type="DOI">10.1136/jmg.2004.022632</idno><idno type="href">jmedgenet-41-900.pdf</idno><idno type="PMID">15591275</idno><idno type="local">0410900</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-2593</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ASP, affected sibling pair</term><term>IBD, identical by descent</term><term>LOD, logarithm of odds</term><term>MLS, maximum LOD score</term><term>Parkinson’s disease</term><term>UPDRS, unified Parkinson’s disease rating score</term><term>genome-wide linkage study</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective: To undertake a full genome-wide screen for Parkinson’s disease susceptibility loci. Methods: A genome-wide linkage study was undertaken in 227 affected sibling pairs from 199 pedigrees with Parkinson’s disease. The pedigree sample consisted of 188 pedigrees from five European countries, and 11 from the USA. Individuals were genotyped for 391 microsatellite markers at ∼10 cM intervals throughout the genome. Multipoint model-free affected sibling pair linkage analyses were carried out using the MLS (maximum LOD score) test. Results: There were six chromosomal regions with maximum MLS peaks of 1 or greater (pointwise p<0.018). Four of these chromosomal regions appear to be newly identified regions, and the highest MLS values were obtained on chromosomes 11q (MLS = 1.60, at 91 cM, D11S4175) and 7p (MLS = 1.51, at 5 cM, D7S531). The remaining two MLS peaks, on 2p11–q12 and 5q23, are consistent with excess sharing in regions reported by other studies. The highest MLS peak was observed on chromosome 2p11–q12 (MLS = 2.04, between markers D2S2216 and D2S160), within a relatively short distance (∼17 cM) from the PARK3 region. Although a stronger support of linkage to this region was observed in the late age of onset subgroup of families, these differences were not significant. The peak on 5q23 (MLS = 1.05, at 130 cM, D5S471) coincides with the region identified by three other genome scans. All peak locations fell within a 10 cM distance. Conclusions: These stratified linkage analyses suggest linkage heterogeneity within the sample across the 2p11–q12 and 5q23 regions, with these two regions contributing independently to Parkinson’s disease susceptibility.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>M Martinez</name><affiliations><json:string>INSERM EMI00-06, Evry, France</json:string></affiliations></json:item><json:item><name>A Brice</name><affiliations><json:string>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>J R Vaughan</name><affiliations><json:string>Department of Neurology Charing Cross Hospital, London, UK</json:string></affiliations></json:item><json:item><name>A Zimprich</name><affiliations><json:string>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</json:string></affiliations></json:item><json:item><name>M M B Breteler</name><affiliations><json:string>Department of Epidemiology and Biostatistics, Erasmus University, Rotterdam, Netherlands</json:string></affiliations></json:item><json:item><name>G Meco</name><affiliations><json:string>Department of Neurological Sciences, La Sapienza University, Rome, Italy</json:string></affiliations></json:item><json:item><name>A Filla</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>M J Farrer</name><affiliations><json:string>Neurogenetics Laboratory, Mayo Clinic Jacksonville, Florida, USA</json:string></affiliations></json:item><json:item><name>C Bétard</name><affiliations><json:string>Centre National de Génotypage, Evry, France</json:string></affiliations></json:item><json:item><name>J Hardy</name><affiliations><json:string>Laboratory of Neurogenetics, National Institute on Aging, NIH, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>G De Michele</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>V Bonifati</name><affiliations><json:string>Department of Neurological Sciences, La Sapienza University, Rome, Italy</json:string></affiliations></json:item><json:item><name>B Oostra</name><affiliations><json:string>Department of Clinical Genetics, Erasmus University, Rotterdam, Netherlands</json:string></affiliations></json:item><json:item><name>T Gasser</name><affiliations><json:string>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</json:string></affiliations></json:item><json:item><name>N W Wood</name><affiliations><json:string>Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK</json:string></affiliations></json:item><json:item><name>A Dürr</name><affiliations><json:string>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Original articles</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Clinical genetics</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Genetic screening / counselling</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ASP, affected sibling pair</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IBD, identical by descent</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LOD, logarithm of odds</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MLS, maximum LOD score</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>UPDRS, unified Parkinson’s disease rating score</value></json:item><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>genome-wide linkage study</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Objective: To undertake a full genome-wide screen for Parkinson’s disease susceptibility loci. Methods: A genome-wide linkage study was undertaken in 227 affected sibling pairs from 199 pedigrees with Parkinson’s disease. The pedigree sample consisted of 188 pedigrees from five European countries, and 11 from the USA. Individuals were genotyped for 391 microsatellite markers at ∼10 cM intervals throughout the genome. Multipoint model-free affected sibling pair linkage analyses were carried out using the MLS (maximum LOD score) test. Results: There were six chromosomal regions with maximum MLS peaks of 1 or greater (pointwise p>0.018). Four of these chromosomal regions appear to be newly identified regions, and the highest MLS values were obtained on chromosomes 11q (MLS = 1.60, at 91 cM, D11S4175) and 7p (MLS = 1.51, at 5 cM, D7S531). The remaining two MLS peaks, on 2p11–q12 and 5q23, are consistent with excess sharing in regions reported by other studies. The highest MLS peak was observed on chromosome 2p11–q12 (MLS = 2.04, between markers D2S2216 and D2S160), within a relatively short distance (∼17 cM) from the PARK3 region. Although a stronger support of linkage to this region was observed in the late age of onset subgroup of families, these differences were not significant. The peak on 5q23 (MLS = 1.05, at 130 cM, D5S471) coincides with the region identified by three other genome scans. All peak locations fell within a 10 cM distance. Conclusions: These stratified linkage analyses suggest linkage heterogeneity within the sample across the 2p11–q12 and 5q23 regions, with these two regions contributing independently to Parkinson’s disease susceptibility.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>10</keywordCount><abstractCharCount>1684</abstractCharCount><pdfWordCount>6675</pdfWordCount><pdfCharCount>42675</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>252</abstractWordCount></qualityIndicators><title>Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease</title><pmid><json:string>15591275</json:string></pmid><genre><json:string>research-article</json:string></genre><host><volume>41</volume><pages><first>900</first></pages><issn><json:string>0022-2593</json:string></issn><issue>12</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-6244</json:string></eissn><title>Journal of Medical Genetics</title></host><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1136/jmg.2004.022632</json:string></doi><id>CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability><p>BMJ</p></availability><date>2004-12-09</date></publicationStmt><notesStmt><note>Correspondence to:
Dr Maria Martinez
Unité de Recherche INSERM EMI00-06, Tour Evry 2, 523 Place des Terrasses de l’Agora, Evry cedex 91068, France; maria@evry.inserm.fr</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease</title><author><persName><forename type="first">M</forename><surname>Martinez</surname></persName><affiliation>INSERM EMI00-06, Evry, France</affiliation></author><author><persName><forename type="first">A</forename><surname>Brice</surname></persName><affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</affiliation></author><author><persName><forename type="first">J R</forename><surname>Vaughan</surname></persName><affiliation>Department of Neurology Charing Cross Hospital, London, UK</affiliation></author><author><persName><forename type="first">A</forename><surname>Zimprich</surname></persName><affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</affiliation></author><author><persName><forename type="first">M M B</forename><surname>Breteler</surname></persName><affiliation>Department of Epidemiology and Biostatistics, Erasmus University, Rotterdam, Netherlands</affiliation></author><author><persName><forename type="first">G</forename><surname>Meco</surname></persName><affiliation>Department of Neurological Sciences, La Sapienza University, Rome, Italy</affiliation></author><author><persName><forename type="first">A</forename><surname>Filla</surname></persName><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">M J</forename><surname>Farrer</surname></persName><affiliation>Neurogenetics Laboratory, Mayo Clinic Jacksonville, Florida, USA</affiliation></author><author><persName><forename type="first">C</forename><surname>Bétard</surname></persName><affiliation>Centre National de Génotypage, Evry, France</affiliation></author><author><persName><forename type="first">J</forename><surname>Hardy</surname></persName><affiliation>Laboratory of Neurogenetics, National Institute on Aging, NIH, Bethesda, Maryland, USA</affiliation></author><author><persName><forename type="first">G</forename><surname>De Michele</surname></persName><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">V</forename><surname>Bonifati</surname></persName><affiliation>Department of Neurological Sciences, La Sapienza University, Rome, Italy</affiliation></author><author><persName><forename type="first">B</forename><surname>Oostra</surname></persName><affiliation>Department of Clinical Genetics, Erasmus University, Rotterdam, Netherlands</affiliation></author><author><persName><forename type="first">T</forename><surname>Gasser</surname></persName><affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</affiliation></author><author><persName><forename type="first">N W</forename><surname>Wood</surname></persName><affiliation>Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK</affiliation></author><author><persName><forename type="first">A</forename><surname>Dürr</surname></persName><affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</affiliation></author></analytic><monogr><title level="j">Journal of Medical Genetics</title><title level="j" type="abbrev">J Med Genet</title><idno type="pISSN">0022-2593</idno><idno type="eISSN">1468-6244</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2004-12"></date><biblScope unit="volume">41</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="900">900</biblScope></imprint></monogr><idno type="istex">CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA</idno><idno type="DOI">10.1136/jmg.2004.022632</idno><idno type="href">jmedgenet-41-900.pdf</idno><idno type="PMID">15591275</idno><idno type="local">0410900</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004-12-09</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objective: To undertake a full genome-wide screen for Parkinson’s disease susceptibility loci. Methods: A genome-wide linkage study was undertaken in 227 affected sibling pairs from 199 pedigrees with Parkinson’s disease. The pedigree sample consisted of 188 pedigrees from five European countries, and 11 from the USA. Individuals were genotyped for 391 microsatellite markers at ∼10 cM intervals throughout the genome. Multipoint model-free affected sibling pair linkage analyses were carried out using the MLS (maximum LOD score) test. Results: There were six chromosomal regions with maximum MLS peaks of 1 or greater (pointwise p<0.018). Four of these chromosomal regions appear to be newly identified regions, and the highest MLS values were obtained on chromosomes 11q (MLS = 1.60, at 91 cM, D11S4175) and 7p (MLS = 1.51, at 5 cM, D7S531). The remaining two MLS peaks, on 2p11–q12 and 5q23, are consistent with excess sharing in regions reported by other studies. The highest MLS peak was observed on chromosome 2p11–q12 (MLS = 2.04, between markers D2S2216 and D2S160), within a relatively short distance (∼17 cM) from the PARK3 region. Although a stronger support of linkage to this region was observed in the late age of onset subgroup of families, these differences were not significant. The peak on 5q23 (MLS = 1.05, at 130 cM, D5S471) coincides with the region identified by three other genome scans. All peak locations fell within a 10 cM distance. Conclusions: These stratified linkage analyses suggest linkage heterogeneity within the sample across the 2p11–q12 and 5q23 regions, with these two regions contributing independently to Parkinson’s disease susceptibility.</p></abstract><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Clinical genetics</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Genetic screening / counselling</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>ASP, affected sibling pair</term></item><item><term>IBD, identical by descent</term></item><item><term>LOD, logarithm of odds</term></item><item><term>MLS, maximum LOD score</term></item><item><term>UPDRS, unified Parkinson’s disease rating score</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>Parkinson’s disease</term></item><item><term>genome-wide linkage study</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-12-09">Created</change><change when="2004-12">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-14">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">jmedgenet</journal-id><journal-id journal-id-type="nlm-ta">J Med Genet</journal-id><journal-title>Journal of Medical Genetics</journal-title><abbrev-journal-title abbrev-type="publisher">J Med Genet</abbrev-journal-title><issn pub-type="ppub">0022-2593</issn><issn pub-type="epub">1468-6244</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">0410900</article-id><article-id pub-id-type="doi">10.1136/jmg.2004.022632</article-id><article-id pub-id-type="other">jmedgenet;41/12/900</article-id><article-id pub-id-type="pmid">15591275</article-id><article-id pub-id-type="other">900</article-id><article-id pub-id-type="other">jmg.2004.022632</article-id><article-categories><subj-group subj-group-type="heading"><subject content-type="original">Original articles</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Clinical genetics</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Genetic screening / counselling</subject></subj-group></article-categories><title-group><article-title>Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Martinez</surname><given-names>M</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Brice</surname><given-names>A</given-names></name><xref rid="AFF2">2</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Vaughan</surname><given-names>J R</given-names></name><xref rid="AFF3">3</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Zimprich</surname><given-names>A</given-names></name><xref rid="AFF4">4</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Breteler</surname><given-names>M M B</given-names></name><xref rid="AFF5">5</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Meco</surname><given-names>G</given-names></name><xref rid="AFF6">6</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Filla</surname><given-names>A</given-names></name><xref rid="AFF7">7</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Farrer</surname><given-names>M J</given-names></name><xref rid="AFF8">8</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Bétard</surname><given-names>C</given-names></name><xref rid="AFF9">9</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hardy</surname><given-names>J</given-names></name><xref rid="AFF10">10</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>De Michele</surname><given-names>G</given-names></name><xref rid="AFF7">7</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Bonifati</surname><given-names>V</given-names></name><xref rid="AFF6">6</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Oostra</surname><given-names>B</given-names></name><xref rid="AFF11">11</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Gasser</surname><given-names>T</given-names></name><xref rid="AFF4">4</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Wood</surname><given-names>N W</given-names></name><xref rid="AFF12">12</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Dürr</surname><given-names>A</given-names></name><xref rid="AFF2">2</xref></contrib><contrib contrib-type="group-author" xlink:type="simple"><on-behalf-of>the French Parkinson’s Disease Genetics Study Group, the European Consortium on Genetic Susceptibility in Parkinson’s Disease</on-behalf-of></contrib><aff id="AFF1"><label>1</label>INSERM EMI00-06, Evry, France</aff><aff id="AFF2"><label>2</label>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</aff><aff id="AFF3"><label>3</label>Department of Neurology Charing Cross Hospital, London, UK</aff><aff id="AFF4"><label>4</label>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</aff><aff id="AFF5"><label>5</label>Department of Epidemiology and Biostatistics, Erasmus University, Rotterdam, Netherlands</aff><aff id="AFF6"><label>6</label>Department of Neurological Sciences, La Sapienza University, Rome, Italy</aff><aff id="AFF7"><label>7</label>Department of Neurological Sciences, Federico II University, Naples, Italy</aff><aff id="AFF8"><label>8</label>Neurogenetics Laboratory, Mayo Clinic Jacksonville, Florida, USA</aff><aff id="AFF9"><label>9</label>Centre National de Génotypage, Evry, France</aff><aff id="AFF10"><label>10</label>Laboratory of Neurogenetics, National Institute on Aging, NIH, Bethesda, Maryland, USA</aff><aff id="AFF11"><label>11</label>Department of Clinical Genetics, Erasmus University, Rotterdam, Netherlands</aff><aff id="AFF12"><label>12</label>Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK</aff></contrib-group><author-notes><corresp>Correspondence to:
Dr Maria Martinez
Unité de Recherche INSERM EMI00-06, Tour Evry 2, 523 Place des Terrasses de l’Agora, Evry cedex 91068, France; <ext-link xlink:href="mariaevry.inserm.fr" ext-link-type="email" xlink:type="simple">maria@evry.inserm.fr</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>12</month><year>2004</year></pub-date><pub-date pub-type="epub"><day>9</day><month>12</month><year>2004</year></pub-date><volume>41</volume><volume-id pub-id-type="other">41</volume-id><volume-id pub-id-type="other">41</volume-id><issue>12</issue><issue-id pub-id-type="other">jmedgenet;41/12</issue-id><issue-id pub-id-type="other">12</issue-id><issue-id pub-id-type="other">41/12</issue-id><fpage>900</fpage><history><date date-type="accepted"><day>30</day><month>06</month><year>2004</year></date><date date-type="rev-recd"><day>29</day><month>06</month><year>2004</year></date></history><permissions><copyright-statement>Copyright 2004 Journal of Medical Genetics</copyright-statement><copyright-year>2004</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jmedgenet-41-900.pdf"></self-uri><abstract xml:lang="en"><p><bold>Objective:</bold> To undertake a full genome-wide screen for Parkinson’s disease susceptibility loci.</p><p><bold>Methods:</bold> A genome-wide linkage study was undertaken in 227 affected sibling pairs from 199 pedigrees with Parkinson’s disease. The pedigree sample consisted of 188 pedigrees from five European countries, and 11 from the USA. Individuals were genotyped for 391 microsatellite markers at ∼10 cM intervals throughout the genome. Multipoint model-free affected sibling pair linkage analyses were carried out using the MLS (maximum LOD score) test.</p><p><bold>Results:</bold> There were six chromosomal regions with maximum MLS peaks of 1 or greater (pointwise p<0.018). Four of these chromosomal regions appear to be newly identified regions, and the highest MLS values were obtained on chromosomes 11q (MLS = 1.60, at 91 cM, D11S4175) and 7p (MLS = 1.51, at 5 cM, D7S531). The remaining two MLS peaks, on 2p11–q12 and 5q23, are consistent with excess sharing in regions reported by other studies. The highest MLS peak was observed on chromosome 2p11–q12 (MLS = 2.04, between markers D2S2216 and D2S160), within a relatively short distance (∼17 cM) from the PARK3 region. Although a stronger support of linkage to this region was observed in the late age of onset subgroup of families, these differences were not significant. The peak on 5q23 (MLS = 1.05, at 130 cM, D5S471) coincides with the region identified by three other genome scans. All peak locations fell within a 10 cM distance.</p><p><bold>Conclusions:</bold> These stratified linkage analyses suggest linkage heterogeneity within the sample across the 2p11–q12 and 5q23 regions, with these two regions contributing independently to Parkinson’s disease susceptibility.</p></abstract><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd>ASP, affected sibling pair</kwd><kwd>IBD, identical by descent</kwd><kwd>LOD, logarithm of odds</kwd><kwd>MLS, maximum LOD score</kwd><kwd>UPDRS, unified Parkinson’s disease rating score</kwd></kwd-group><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>Parkinson’s disease</kwd><kwd>genome-wide linkage study</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Genome-wide scan linkage analysis for Parkinson’s disease: the European genetic study of Parkinson’s disease</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Martinez</namePart><affiliation>INSERM EMI00-06, Evry, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Brice</namePart><affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J R</namePart><namePart type="family">Vaughan</namePart><affiliation>Department of Neurology Charing Cross Hospital, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Zimprich</namePart><affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M M B</namePart><namePart type="family">Breteler</namePart><affiliation>Department of Epidemiology and Biostatistics, Erasmus University, Rotterdam, Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Meco</namePart><affiliation>Department of Neurological Sciences, La Sapienza University, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Filla</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M J</namePart><namePart type="family">Farrer</namePart><affiliation>Neurogenetics Laboratory, Mayo Clinic Jacksonville, Florida, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Bétard</namePart><affiliation>Centre National de Génotypage, Evry, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Hardy</namePart><affiliation>Laboratory of Neurogenetics, National Institute on Aging, NIH, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">De Michele</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Bonifati</namePart><affiliation>Department of Neurological Sciences, La Sapienza University, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Oostra</namePart><affiliation>Department of Clinical Genetics, Erasmus University, Rotterdam, Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Gasser</namePart><affiliation>Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N W</namePart><namePart type="family">Wood</namePart><affiliation>Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Dürr</namePart><affiliation>INSERM U289 and Département de Génétique, Cytogénétique et Embryologie, Hôpital La Pitité-Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><genre>hwp-journal-coll</genre><topic>Clinical genetics</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Genetic screening / counselling</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2004-12</dateIssued><dateCreated encoding="w3cdtf">2004-12-09</dateCreated><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Objective: To undertake a full genome-wide screen for Parkinson’s disease susceptibility loci. Methods: A genome-wide linkage study was undertaken in 227 affected sibling pairs from 199 pedigrees with Parkinson’s disease. The pedigree sample consisted of 188 pedigrees from five European countries, and 11 from the USA. Individuals were genotyped for 391 microsatellite markers at ∼10 cM intervals throughout the genome. Multipoint model-free affected sibling pair linkage analyses were carried out using the MLS (maximum LOD score) test. Results: There were six chromosomal regions with maximum MLS peaks of 1 or greater (pointwise p<0.018). Four of these chromosomal regions appear to be newly identified regions, and the highest MLS values were obtained on chromosomes 11q (MLS = 1.60, at 91 cM, D11S4175) and 7p (MLS = 1.51, at 5 cM, D7S531). The remaining two MLS peaks, on 2p11–q12 and 5q23, are consistent with excess sharing in regions reported by other studies. The highest MLS peak was observed on chromosome 2p11–q12 (MLS = 2.04, between markers D2S2216 and D2S160), within a relatively short distance (∼17 cM) from the PARK3 region. Although a stronger support of linkage to this region was observed in the late age of onset subgroup of families, these differences were not significant. The peak on 5q23 (MLS = 1.05, at 130 cM, D5S471) coincides with the region identified by three other genome scans. All peak locations fell within a 10 cM distance. Conclusions: These stratified linkage analyses suggest linkage heterogeneity within the sample across the 2p11–q12 and 5q23 regions, with these two regions contributing independently to Parkinson’s disease susceptibility.</abstract><note type="author-notes">Correspondence to:
Dr Maria Martinez
Unité de Recherche INSERM EMI00-06, Tour Evry 2, 523 Place des Terrasses de l’Agora, Evry cedex 91068, France; maria@evry.inserm.fr</note><subject lang="en"><genre>ABR</genre><topic>ASP, affected sibling pair</topic><topic>IBD, identical by descent</topic><topic>LOD, logarithm of odds</topic><topic>MLS, maximum LOD score</topic><topic>UPDRS, unified Parkinson’s disease rating score</topic></subject><subject lang="en"><genre>KWD</genre><topic>Parkinson’s disease</topic><topic>genome-wide linkage study</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Genetics</title></titleInfo><titleInfo type="abbreviated"><title>J Med Genet</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-2593</identifier><identifier type="eISSN">1468-6244</identifier><identifier type="PublisherID-hwp">jmedgenet</identifier><identifier type="PublisherID-nlm-ta">J Med Genet</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>41</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>900</start></extent></part></relatedItem><identifier type="istex">CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA</identifier><identifier type="DOI">10.1136/jmg.2004.022632</identifier><identifier type="href">jmedgenet-41-900.pdf</identifier><identifier type="PMID">15591275</identifier><identifier type="local">0410900</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright 2004 Journal of Medical Genetics</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/CF7DE1EBF8B02E29DAEC73DA3BE5D97BE61586DA/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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