Association analysis of MAPT H1 haplotype and subhaplotypes in Parkinson's disease
Identifieur interne : 001E87 ( Main/Corpus ); précédent : 001E86; suivant : 001E88Association analysis of MAPT H1 haplotype and subhaplotypes in Parkinson's disease
Auteurs : Cyrus P. Zabetian ; Carolyn M. Hutter ; Stewart A. Factor ; John G. Nutt ; Donald S. Higgins ; Alida Griffith ; John W. Roberts ; Berta C. Leis ; Denise M. Kay ; Dora Yearout ; Jennifer S. Montimurro ; Karen L. Edwards ; Ali Samii ; Haydeh PayamiSource :
- Annals of Neurology [ 0364-5134 ] ; 2007-08.
Abstract
Objective: An inversion polymorphism of approximately 900kb on chromosome 17q21, which includes the microtubule‐associated protein tau (MAPT) gene defines two haplotype clades, H1 and H2. Several small case–control studies have observed a marginally significant excess of the H1/H1 diplotype among patients with Parkinson's disease (PD), and one reported refining the association to a region spanning exons 1 to 4 of MAPT. We sought to replicate these findings. Methods: We genotyped 1,762 PD patients and 2,010 control subjects for a single nucleotide polymorphism (SNP) that differentiates the H1 and H2 clades. We also analyzed four SNPs that define subhaplotypes within H1 previously reported to associate with PD or other neurodegenerative disorders. Results: After adjusting for age, sex, and site, we observed a robust association between the H1/H1 diplotype and PD risk (odds ratio for H1/H1 vs H1/H2 and H2/H2, 1.46; 95% confidence interval, 1.25–1.69; p = 8 × 10−7). The effect was evident in both familial and sporadic subgroups, men and women, and early‐ and late‐onset disease. Within H1/H1 individuals, there was no significant difference between cases and control subjects in the overall frequency distribution of H1 subhaplotypes. Interpretation: Our data provide strong evidence that the H1 clade, which contains MAPT and several other genes, is a risk factor for PD. However, attributing this finding to variants within a specific region of MAPT is premature. Thorough fine‐mapping of the H1 clade in large numbers of individuals is now needed to identify the underlying functional variant(s) that alter susceptibility for PD. Ann Neurol 2007
Url:
DOI: 10.1002/ana.21157
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Zabetian</name><affiliation><mods:affiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Hutter, Carolyn M" sort="Hutter, Carolyn M" uniqKey="Hutter C" first="Carolyn M." last="Hutter">Carolyn M. Hutter</name><affiliation><mods:affiliation>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Factor, Stewart A" sort="Factor, Stewart A" uniqKey="Factor S" first="Stewart A." last="Factor">Stewart A. Factor</name><affiliation><mods:affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</mods:affiliation></affiliation></author><author><name sortKey="Nutt, John G" sort="Nutt, John G" uniqKey="Nutt J" first="John G." last="Nutt">John G. Nutt</name><affiliation><mods:affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</mods:affiliation></affiliation></author><author><name sortKey="Higgins, Donald S" sort="Higgins, Donald S" uniqKey="Higgins D" first="Donald S." last="Higgins">Donald S. Higgins</name><affiliation><mods:affiliation>Parkinson's Disease and Movement Disorder Clinic, Albany Medical Center, Albany, NY</mods:affiliation></affiliation></author><author><name sortKey="Griffith, Alida" sort="Griffith, Alida" uniqKey="Griffith A" first="Alida" last="Griffith">Alida Griffith</name><affiliation><mods:affiliation>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</mods:affiliation></affiliation></author><author><name sortKey="Roberts, John W" sort="Roberts, John W" uniqKey="Roberts J" first="John W." last="Roberts">John W. Roberts</name><affiliation><mods:affiliation>Virginia Mason Medical Center, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Leis, Berta C" sort="Leis, Berta C" uniqKey="Leis B" first="Berta C." last="Leis">Berta C. Leis</name><affiliation><mods:affiliation>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</mods:affiliation></affiliation></author><author><name sortKey="Kay, Denise M" sort="Kay, Denise M" uniqKey="Kay D" first="Denise M." last="Kay">Denise M. Kay</name><affiliation><mods:affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</mods:affiliation></affiliation></author><author><name sortKey="Yearout, Dora" sort="Yearout, Dora" uniqKey="Yearout D" first="Dora" last="Yearout">Dora Yearout</name><affiliation><mods:affiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Montimurro, Jennifer S" sort="Montimurro, Jennifer S" uniqKey="Montimurro J" first="Jennifer S." last="Montimurro">Jennifer S. Montimurro</name><affiliation><mods:affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</mods:affiliation></affiliation></author><author><name sortKey="Edwards, Karen L" sort="Edwards, Karen L" uniqKey="Edwards K" first="Karen L." last="Edwards">Karen L. Edwards</name><affiliation><mods:affiliation>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Samii, Ali" sort="Samii, Ali" uniqKey="Samii A" first="Ali" last="Samii">Ali Samii</name><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Parkinson's Disease Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Payami, Haydeh" sort="Payami, Haydeh" uniqKey="Payami H" first="Haydeh" last="Payami">Haydeh Payami</name><affiliation><mods:affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-08">2007-08</date><biblScope unit="volume">62</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="137">137</biblScope><biblScope unit="page" to="144">144</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">628B0AEC8BBF33DEC594591A957764CA7BA89847</idno><idno type="DOI">10.1002/ana.21157</idno><idno type="ArticleID">ANA21157</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective: An inversion polymorphism of approximately 900kb on chromosome 17q21, which includes the microtubule‐associated protein tau (MAPT) gene defines two haplotype clades, H1 and H2. Several small case–control studies have observed a marginally significant excess of the H1/H1 diplotype among patients with Parkinson's disease (PD), and one reported refining the association to a region spanning exons 1 to 4 of MAPT. We sought to replicate these findings. Methods: We genotyped 1,762 PD patients and 2,010 control subjects for a single nucleotide polymorphism (SNP) that differentiates the H1 and H2 clades. We also analyzed four SNPs that define subhaplotypes within H1 previously reported to associate with PD or other neurodegenerative disorders. Results: After adjusting for age, sex, and site, we observed a robust association between the H1/H1 diplotype and PD risk (odds ratio for H1/H1 vs H1/H2 and H2/H2, 1.46; 95% confidence interval, 1.25–1.69; p = 8 × 10−7). The effect was evident in both familial and sporadic subgroups, men and women, and early‐ and late‐onset disease. Within H1/H1 individuals, there was no significant difference between cases and control subjects in the overall frequency distribution of H1 subhaplotypes. Interpretation: Our data provide strong evidence that the H1 clade, which contains MAPT and several other genes, is a risk factor for PD. However, attributing this finding to variants within a specific region of MAPT is premature. Thorough fine‐mapping of the H1 clade in large numbers of individuals is now needed to identify the underlying functional variant(s) that alter susceptibility for PD. Ann Neurol 2007</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Cyrus P. Zabetian MD, MS</name><affiliations><json:string>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Carolyn M. Hutter MS</name><affiliations><json:string>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Stewart A. Factor DO</name><affiliations><json:string>Department of Neurology, Emory University School of Medicine, Atlanta, GA</json:string></affiliations></json:item><json:item><name>John G. Nutt MD</name><affiliations><json:string>Department of Neurology, Oregon Health and Science University, Portland, OR</json:string></affiliations></json:item><json:item><name>Donald S. Higgins MD</name><affiliations><json:string>Parkinson's Disease and Movement Disorder Clinic, Albany Medical Center, Albany, NY</json:string></affiliations></json:item><json:item><name>Alida Griffith MD</name><affiliations><json:string>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</json:string></affiliations></json:item><json:item><name>John W. Roberts MD</name><affiliations><json:string>Virginia Mason Medical Center, Seattle, WA</json:string></affiliations></json:item><json:item><name>Berta C. Leis RN, PhD</name><affiliations><json:string>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</json:string></affiliations></json:item><json:item><name>Denise M. Kay PhD</name><affiliations><json:string>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</json:string></affiliations></json:item><json:item><name>Dora Yearout BS</name><affiliations><json:string>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Jennifer S. Montimurro BS</name><affiliations><json:string>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</json:string></affiliations></json:item><json:item><name>Karen L. Edwards PhD</name><affiliations><json:string>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Ali Samii MD</name><affiliations><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, WA</json:string><json:string>Parkinson's Disease Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</json:string></affiliations></json:item><json:item><name>Haydeh Payami PhD</name><affiliations><json:string>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</json:string></affiliations></json:item></author><articleId><json:string>ANA21157</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objective: An inversion polymorphism of approximately 900kb on chromosome 17q21, which includes the microtubule‐associated protein tau (MAPT) gene defines two haplotype clades, H1 and H2. Several small case–control studies have observed a marginally significant excess of the H1/H1 diplotype among patients with Parkinson's disease (PD), and one reported refining the association to a region spanning exons 1 to 4 of MAPT. We sought to replicate these findings. Methods: We genotyped 1,762 PD patients and 2,010 control subjects for a single nucleotide polymorphism (SNP) that differentiates the H1 and H2 clades. We also analyzed four SNPs that define subhaplotypes within H1 previously reported to associate with PD or other neurodegenerative disorders. Results: After adjusting for age, sex, and site, we observed a robust association between the H1/H1 diplotype and PD risk (odds ratio for H1/H1 vs H1/H2 and H2/H2, 1.46; 95% confidence interval, 1.25–1.69; p = 8 × 10−7). The effect was evident in both familial and sporadic subgroups, men and women, and early‐ and late‐onset disease. Within H1/H1 individuals, there was no significant difference between cases and control subjects in the overall frequency distribution of H1 subhaplotypes. Interpretation: Our data provide strong evidence that the H1 clade, which contains MAPT and several other genes, is a risk factor for PD. However, attributing this finding to variants within a specific region of MAPT is premature. Thorough fine‐mapping of the H1 clade in large numbers of individuals is now needed to identify the underlying functional variant(s) that alter susceptibility for PD. Ann Neurol 2007</abstract><qualityIndicators><score>7.733</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 783 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1660</abstractCharCount><pdfWordCount>4733</pdfWordCount><pdfCharCount>30235</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>252</abstractWordCount></qualityIndicators><title>Association analysis of MAPT H1 haplotype and subhaplotypes in Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>62</volume><publisherId><json:string>ANA</json:string></publisherId><pages><total>8</total><last>144</last><first>137</first></pages><issn><json:string>0364-5134</json:string></issn><issue>2</issue><subject><json:item><value>Original Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8249</json:string></eissn><title>Annals of Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1002/ana.21157</json:string></doi><id>628B0AEC8BBF33DEC594591A957764CA7BA89847</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/628B0AEC8BBF33DEC594591A957764CA7BA89847/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/628B0AEC8BBF33DEC594591A957764CA7BA89847/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/628B0AEC8BBF33DEC594591A957764CA7BA89847/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Association analysis of MAPT H1 haplotype and subhaplotypes in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2007</date></publicationStmt><notesStmt><note>Michael J. Fox Foundation (Edmond J. Safra Global Genetics Consortia Initiative)</note><note>NIH - No. NINDS, K08 NS044138; No. N1A P30 AG008017; No. NINDS, R01 NS036960;</note><note>Department of Veterans Affairs Merit Review Award</note><note>Veterans Integrated Service Network 20 Geriatric, Mental Illness</note><note>Parkinson's Disease Research Education and Clinical Centers</note><note>Wadsworth Center, New York State Department of Health</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Association analysis of MAPT H1 haplotype and subhaplotypes in Parkinson's disease</title><author><persName><forename type="first">Cyrus P.</forename><surname>Zabetian</surname></persName><roleName type="degree">MD, MS</roleName><note type="correspondence"><p>Correspondence: Geriatric Research Education and Clinical Center S‐182, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108</p></note><affiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Carolyn M.</forename><surname>Hutter</surname></persName><roleName type="degree">MS</roleName><affiliation>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Stewart A.</forename><surname>Factor</surname></persName><roleName type="degree">DO</roleName><affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</affiliation></author><author><persName><forename type="first">John G.</forename><surname>Nutt</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</affiliation></author><author><persName><forename type="first">Donald S.</forename><surname>Higgins</surname></persName><roleName type="degree">MD</roleName><affiliation>Parkinson's Disease and Movement Disorder Clinic, Albany Medical Center, Albany, NY</affiliation></author><author><persName><forename type="first">Alida</forename><surname>Griffith</surname></persName><roleName type="degree">MD</roleName><affiliation>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</affiliation></author><author><persName><forename type="first">John W.</forename><surname>Roberts</surname></persName><roleName type="degree">MD</roleName><affiliation>Virginia Mason Medical Center, Seattle, WA</affiliation></author><author><persName><forename type="first">Berta C.</forename><surname>Leis</surname></persName><roleName type="degree">RN, PhD</roleName><affiliation>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</affiliation></author><author><persName><forename type="first">Denise M.</forename><surname>Kay</surname></persName><roleName type="degree">PhD</roleName><affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</affiliation></author><author><persName><forename type="first">Dora</forename><surname>Yearout</surname></persName><roleName type="degree">BS</roleName><affiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Jennifer S.</forename><surname>Montimurro</surname></persName><roleName type="degree">BS</roleName><affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</affiliation></author><author><persName><forename type="first">Karen L.</forename><surname>Edwards</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Ali</forename><surname>Samii</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Parkinson's Disease Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation></author><author><persName><forename type="first">Haydeh</forename><surname>Payami</surname></persName><roleName type="degree">PhD</roleName><affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-08"></date><biblScope unit="volume">62</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="137">137</biblScope><biblScope unit="page" to="144">144</biblScope></imprint></monogr><idno type="istex">628B0AEC8BBF33DEC594591A957764CA7BA89847</idno><idno type="DOI">10.1002/ana.21157</idno><idno type="ArticleID">ANA21157</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objective: An inversion polymorphism of approximately 900kb on chromosome 17q21, which includes the microtubule‐associated protein tau (MAPT) gene defines two haplotype clades, H1 and H2. Several small case–control studies have observed a marginally significant excess of the H1/H1 diplotype among patients with Parkinson's disease (PD), and one reported refining the association to a region spanning exons 1 to 4 of MAPT. We sought to replicate these findings. Methods: We genotyped 1,762 PD patients and 2,010 control subjects for a single nucleotide polymorphism (SNP) that differentiates the H1 and H2 clades. We also analyzed four SNPs that define subhaplotypes within H1 previously reported to associate with PD or other neurodegenerative disorders. Results: After adjusting for age, sex, and site, we observed a robust association between the H1/H1 diplotype and PD risk (odds ratio for H1/H1 vs H1/H2 and H2/H2, 1.46; 95% confidence interval, 1.25–1.69; p = 8 × 10−7). The effect was evident in both familial and sporadic subgroups, men and women, and early‐ and late‐onset disease. Within H1/H1 individuals, there was no significant difference between cases and control subjects in the overall frequency distribution of H1 subhaplotypes. Interpretation: Our data provide strong evidence that the H1 clade, which contains MAPT and several other genes, is a risk factor for PD. However, attributing this finding to variants within a specific region of MAPT is premature. Thorough fine‐mapping of the H1 clade in large numbers of individuals is now needed to identify the underlying functional variant(s) that alter susceptibility for PD. Ann Neurol 2007</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-12-07">Received</change><change when="2007-04-16">Registration</change><change when="2007-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/628B0AEC8BBF33DEC594591A957764CA7BA89847/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 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number="8"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2007 American Neurological Association</copyright><eventGroup><event type="manuscriptReceived" date="2006-12-07"></event><event type="manuscriptRevised" date="2007-04-13"></event><event type="manuscriptAccepted" date="2007-04-16"></event><event type="firstOnline" date="2007-05-18"></event><event type="publishedOnlineFinalForm" date="2007-09-19"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2007-05-18"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.1.6 mode:FullText" date="2012-09-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></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">137</numbering><numbering type="pageLast">144</numbering></numberingGroup><correspondenceTo>Geriatric Research Education and Clinical Center S‐182, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108</correspondenceTo><objectNameGroup><objectName elementName="figure">Illustration</objectName></objectNameGroup><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA21157.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="44"></count><count type="wordTotal" number="5600"></count></countGroup><titleGroup><title type="main" xml:lang="en">Association analysis of <i>MAPT</i> H1 haplotype and subhaplotypes in Parkinson's disease</title><title type="short" xml:lang="en"><fi>MAPT</fi> in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Cyrus P.</givenNames><familyName>Zabetian</familyName><degrees>MD, MS</degrees></personName><contactDetails><email>zabetian@u.washington.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Carolyn M.</givenNames><familyName>Hutter</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Stewart A.</givenNames><familyName>Factor</familyName><degrees>DO</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af5"><personName><givenNames>John G.</givenNames><familyName>Nutt</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Donald S.</givenNames><familyName>Higgins</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af7"><personName><givenNames>Alida</givenNames><familyName>Griffith</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af8"><personName><givenNames>John W.</givenNames><familyName>Roberts</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af7"><personName><givenNames>Berta C.</givenNames><familyName>Leis</familyName><degrees>RN, PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af9"><personName><givenNames>Denise M.</givenNames><familyName>Kay</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Dora</givenNames><familyName>Yearout</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af9"><personName><givenNames>Jennifer S.</givenNames><familyName>Montimurro</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Karen L.</givenNames><familyName>Edwards</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au13" creatorRole="author" affiliationRef="#af2 #af10"><personName><givenNames>Ali</givenNames><familyName>Samii</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au14" creatorRole="author" affiliationRef="#af9"><personName><givenNames>Haydeh</givenNames><familyName>Payami</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Parkinson's Disease and Movement Disorder Clinic, Albany Medical Center, Albany, NY</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="US" type="organization"><unparsedAffiliation>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="US" type="organization"><unparsedAffiliation>Virginia Mason Medical Center, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af9" countryCode="US" type="organization"><unparsedAffiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</unparsedAffiliation></affiliation><affiliation xml:id="af10" countryCode="US" type="organization"><unparsedAffiliation>Parkinson's Disease Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>Michael J. Fox Foundation (Edmond J. Safra Global Genetics Consortia Initiative)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>NIH</fundingAgency><fundingNumber>NINDS, K08 NS044138</fundingNumber><fundingNumber>N1A P30 AG008017</fundingNumber><fundingNumber>NINDS, R01 NS036960</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Department of Veterans Affairs Merit Review Award</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Veterans Integrated Service Network 20 Geriatric, Mental Illness</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Parkinson's Disease Research Education and Clinical Centers</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Wadsworth Center, New York State Department of Health</fundingAgency></fundingInfo><supportingInformation><p> This article includes supplementary materials available via the Internet at <url href="http://www.interscience.wiley.com/jpages/0364-5134/suppmat"> http://www.interscience.wiley.com/jpages/0364‐5134/suppmat </url></p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana21157:ANA21157_SuppTable1"></mediaResource><caption>Supporting Information file ANA21157_SuppTable1.doc</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana21157:ANA21157_SuppTable2"></mediaResource><caption>Supporting Information file ANA21157_SuppTable2.doc</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Objective</title><p>An inversion polymorphism of approximately 900kb on chromosome 17q21, which includes the microtubule‐associated protein tau (<i>MAPT</i>) gene defines two haplotype clades, H1 and H2. Several small case–control studies have observed a marginally significant excess of the H1/H1 diplotype among patients with Parkinson's disease (PD), and one reported refining the association to a region spanning exons 1 to 4 of <i>MAPT</i>. We sought to replicate these findings.</p></section><section xml:id="abs1-2"><title type="main">Methods</title><p>We genotyped 1,762 PD patients and 2,010 control subjects for a single nucleotide polymorphism (SNP) that differentiates the H1 and H2 clades. We also analyzed four SNPs that define subhaplotypes within H1 previously reported to associate with PD or other neurodegenerative disorders.</p></section><section xml:id="abs1-3"><title type="main">Results</title><p>After adjusting for age, sex, and site, we observed a robust association between the H1/H1 diplotype and PD risk (odds ratio for H1/H1 vs H1/H2 and H2/H2, 1.46; 95% confidence interval, 1.25–1.69; <i>p</i> = 8 × 10<sup>−7</sup>). The effect was evident in both familial and sporadic subgroups, men and women, and early‐ and late‐onset disease. Within H1/H1 individuals, there was no significant difference between cases and control subjects in the overall frequency distribution of H1 subhaplotypes.</p></section><section xml:id="abs1-4"><title type="main">Interpretation</title><p>Our data provide strong evidence that the H1 clade, which contains <i>MAPT</i> and several other genes, is a risk factor for PD. However, attributing this finding to variants within a specific region of <i>MAPT</i> is premature. Thorough fine‐mapping of the H1 clade in large numbers of individuals is now needed to identify the underlying functional variant(s) that alter susceptibility for PD. Ann Neurol 2007</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Association analysis of MAPT H1 haplotype and subhaplotypes in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>MAPT in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Association analysis of</title></titleInfo><name type="personal"><namePart type="given">Cyrus P.</namePart><namePart type="family">Zabetian</namePart><namePart type="termsOfAddress">MD, MS</namePart><affiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation><description>Correspondence: Geriatric Research Education and Clinical Center S‐182, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carolyn M.</namePart><namePart type="family">Hutter</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stewart A.</namePart><namePart type="family">Factor</namePart><namePart type="termsOfAddress">DO</namePart><affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John G.</namePart><namePart type="family">Nutt</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donald S.</namePart><namePart type="family">Higgins</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson's Disease and Movement Disorder Clinic, Albany Medical Center, Albany, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alida</namePart><namePart type="family">Griffith</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John W.</namePart><namePart type="family">Roberts</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Virginia Mason Medical Center, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Berta C.</namePart><namePart type="family">Leis</namePart><namePart type="termsOfAddress">RN, PhD</namePart><affiliation>Booth Gardner Parkinson's Care Center, Evergreen Hospital Medical Center, Kirkland, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Denise M.</namePart><namePart type="family">Kay</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dora</namePart><namePart type="family">Yearout</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jennifer S.</namePart><namePart type="family">Montimurro</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karen L.</namePart><namePart type="family">Edwards</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Epidemiology, University of Washington School of Public Health and Community Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ali</namePart><namePart type="family">Samii</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Parkinson's Disease Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Haydeh</namePart><namePart type="family">Payami</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Genomics Institute, Wadsworth Center, New York State Department of Health, Albany, NY</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">2007-08</dateIssued><dateCaptured encoding="w3cdtf">2006-12-07</dateCaptured><dateValid encoding="w3cdtf">2007-04-16</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">3</extent><extent unit="references">44</extent><extent unit="words">5600</extent></physicalDescription><abstract lang="en">Objective: An inversion polymorphism of approximately 900kb on chromosome 17q21, which includes the microtubule‐associated protein tau (MAPT) gene defines two haplotype clades, H1 and H2. Several small case–control studies have observed a marginally significant excess of the H1/H1 diplotype among patients with Parkinson's disease (PD), and one reported refining the association to a region spanning exons 1 to 4 of MAPT. We sought to replicate these findings. Methods: We genotyped 1,762 PD patients and 2,010 control subjects for a single nucleotide polymorphism (SNP) that differentiates the H1 and H2 clades. We also analyzed four SNPs that define subhaplotypes within H1 previously reported to associate with PD or other neurodegenerative disorders. Results: After adjusting for age, sex, and site, we observed a robust association between the H1/H1 diplotype and PD risk (odds ratio for H1/H1 vs H1/H2 and H2/H2, 1.46; 95% confidence interval, 1.25–1.69; p = 8 × 10−7). The effect was evident in both familial and sporadic subgroups, men and women, and early‐ and late‐onset disease. Within H1/H1 individuals, there was no significant difference between cases and control subjects in the overall frequency distribution of H1 subhaplotypes. Interpretation: Our data provide strong evidence that the H1 clade, which contains MAPT and several other genes, is a risk factor for PD. However, attributing this finding to variants within a specific region of MAPT is premature. Thorough fine‐mapping of the H1 clade in large numbers of individuals is now needed to identify the underlying functional variant(s) that alter susceptibility for PD. Ann Neurol 2007</abstract><note type="funding">Michael J. Fox Foundation (Edmond J. Safra Global Genetics Consortia Initiative)</note><note type="funding">NIH - No. NINDS, K08 NS044138; No. N1A P30 AG008017; No. NINDS, R01 NS036960; </note><note type="funding">Department of Veterans Affairs Merit Review Award</note><note type="funding">Veterans Integrated Service Network 20 Geriatric, Mental Illness</note><note type="funding">Parkinson's Disease Research Education and Clinical Centers</note><note type="funding">Wadsworth Center, New York State Department of Health</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> This article includes supplementary materials available via the Internet at http://www.interscience.wiley.com/jpages/0364‐5134/suppmatSupporting Info Item: Supporting Information file ANA21157_SuppTable1.doc - Supporting Information file ANA21157_SuppTable2.doc - </note><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>62</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>137</start><end>144</end><total>8</total></extent></part></relatedItem><identifier type="istex">628B0AEC8BBF33DEC594591A957764CA7BA89847</identifier><identifier type="DOI">10.1002/ana.21157</identifier><identifier type="ArticleID">ANA21157</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 American Neurological Association</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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