Family‐based case–control study of MAOA and MAOB polymorphisms in Parkinson disease
Identifieur interne : 001337 ( Main/Corpus ); précédent : 001336; suivant : 001338Family‐based case–control study of MAOA and MAOB polymorphisms in Parkinson disease
Auteurs : Sun J. Kang ; William K. Scott ; Yi-Ju Li ; Michael A. Hauser ; Joelle M. Van Der Walt ; Kenichiro Fujiwara ; Gregory M. Mayhew ; Sandra G. West ; Jeffery M. Vance ; Eden R. MartinSource :
- Movement Disorders [ 0885-3185 ] ; 2006-12.
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- KwdEn :
Abstract
Monoamine oxidase (MAO) is an enzyme regulating metabolism of neurotransmitters such as dopamine. Two distinct forms of enzyme, encoded by genes MAOA and MAOB located on the X chromosome, have been considered as possible factors in the pathogenesis of Parkinson disease (PD). Previous association studies of PD and MAO genes reported inconsistent results. In this study, we used a large family‐based data set to test associations between MAO genes and a risk of PD. The data set includes 298 female discordant sibpairs and 348 male discordant sibpairs. For this study, all subjects analyzed were white and families with known parkin mutations were removed. We analyzed 15 single nucleotide polymorphisms (SNPs) and a dinucleotide repeat marker in the MAO genes. Association was found with the intron 13 SNP of MAOB in the female subset (P = 0.02). No significant association was found in the male subset. Our results add to the evidence of involvement of MAOB in PD and suggest that the effect may be stronger in women. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21151
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Two distinct forms of enzyme, encoded by genes MAOA and MAOB located on the X chromosome, have been considered as possible factors in the pathogenesis of Parkinson disease (PD). Previous association studies of PD and MAO genes reported inconsistent results. In this study, we used a large family‐based data set to test associations between MAO genes and a risk of PD. The data set includes 298 female discordant sibpairs and 348 male discordant sibpairs. For this study, all subjects analyzed were white and families with known parkin mutations were removed. We analyzed 15 single nucleotide polymorphisms (SNPs) and a dinucleotide repeat marker in the MAO genes. Association was found with the intron 13 SNP of MAOB in the female subset (P = 0.02). No significant association was found in the male subset. Our results add to the evidence of involvement of MAOB in PD and suggest that the effect may be stronger in women. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Sun J. Kang PhD</name><affiliations><json:string>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</json:string><json:string>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</json:string></affiliations></json:item><json:item><name>William K. 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Mayhew MS</name><affiliations><json:string>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</json:string></affiliations></json:item><json:item><name>Sandra G. West BS</name><affiliations><json:string>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</json:string></affiliations></json:item><json:item><name>Jeffery M. Vance MD, PhD</name><affiliations><json:string>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</json:string><json:string>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</json:string></affiliations></json:item><json:item><name>Eden R. 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Our results add to the evidence of involvement of MAOB in PD and suggest that the effect may be stronger in women. © 2006 Movement Disorder Society</abstract><qualityIndicators><score>5.738</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1052</abstractCharCount><pdfWordCount>3674</pdfWordCount><pdfCharCount>22761</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>172</abstractWordCount></qualityIndicators><title>Family‐based case–control study of MAOA and MAOB polymorphisms in Parkinson disease</title><genre><json:string>article</json:string></genre><host><volume>21</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>6</total><last>2180</last><first>2175</first></pages><issn><json:string>0885-3185</json:string></issn><issue>12</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1002/mds.21151</json:string></doi><id>F5A10EB001E33C6DB921F3F2610F89C2719BEF62</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/F5A10EB001E33C6DB921F3F2610F89C2719BEF62/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/F5A10EB001E33C6DB921F3F2610F89C2719BEF62/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/F5A10EB001E33C6DB921F3F2610F89C2719BEF62/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Family‐based case–control study of MAOA and MAOB polymorphisms in Parkinson 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>2006</date></publicationStmt><notesStmt><note>National Institutes of Health - No. NS39764; 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Two distinct forms of enzyme, encoded by genes MAOA and MAOB located on the X chromosome, have been considered as possible factors in the pathogenesis of Parkinson disease (PD). Previous association studies of PD and MAO genes reported inconsistent results. In this study, we used a large family‐based data set to test associations between MAO genes and a risk of PD. The data set includes 298 female discordant sibpairs and 348 male discordant sibpairs. For this study, all subjects analyzed were white and families with known parkin mutations were removed. We analyzed 15 single nucleotide polymorphisms (SNPs) and a dinucleotide repeat marker in the MAO genes. Association was found with the intron 13 SNP of MAOB in the female subset (P = 0.02). No significant association was found in the male subset. Our results add to the evidence of involvement of MAOB in PD and suggest that the effect may be stronger in women. © 2006 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>PD</term></item><item><term>MAOA</term></item><item><term>MAOB</term></item><item><term>family‐based association</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-03-16">Received</change><change when="2006-07-05">Registration</change><change when="2006-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F5A10EB001E33C6DB921F3F2610F89C2719BEF62/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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href="file:MDS.MDS21151.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="4"></count><count type="referenceTotal" number="22"></count><count type="wordTotal" number="4244"></count></countGroup><titleGroup><title type="main" xml:lang="en">Family‐based case–control study of MAOA and MAOB polymorphisms in Parkinson disease</title><title type="short" xml:lang="en">Family‐Based Study of MAO</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Sun J.</givenNames><familyName>Kang</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>William K.</givenNames><familyName>Scott</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Yi‐Ju</givenNames><familyName>Li</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Michael A.</givenNames><familyName>Hauser</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Joelle M.</givenNames><familyName>van der Walt</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Kenichiro</givenNames><familyName>Fujiwara</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Gregory M.</givenNames><familyName>Mayhew</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Sandra G.</givenNames><familyName>West</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Jeffery M.</givenNames><familyName>Vance</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Eden R.</givenNames><familyName>Martin</familyName><degrees>PhD</degrees></personName><contactDetails><email>emartin@chg.duhs.duke.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">PD</keyword><keyword xml:id="kwd2">MAOA</keyword><keyword xml:id="kwd3">MAOB</keyword><keyword xml:id="kwd4">family‐based association</keyword></keywordGroup><fundingInfo><fundingAgency>National Institutes of Health</fundingAgency><fundingNumber>NS39764</fundingNumber><fundingNumber>NS051355</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Monoamine oxidase (MAO) is an enzyme regulating metabolism of neurotransmitters such as dopamine. Two distinct forms of enzyme, encoded by genes MAOA and MAOB located on the X chromosome, have been considered as possible factors in the pathogenesis of Parkinson disease (PD). Previous association studies of PD and MAO genes reported inconsistent results. In this study, we used a large family‐based data set to test associations between MAO genes and a risk of PD. The data set includes 298 female discordant sibpairs and 348 male discordant sibpairs. For this study, all subjects analyzed were white and families with known parkin mutations were removed. We analyzed 15 single nucleotide polymorphisms (SNPs) and a dinucleotide repeat marker in the MAO genes. Association was found with the intron 13 SNP of MAOB in the female subset (<i>P</i> = 0.02). No significant association was found in the male subset. Our results add to the evidence of involvement of MAOB in PD and suggest that the effect may be stronger in women. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Family‐based case–control study of MAOA and MAOB polymorphisms in Parkinson disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Family‐Based Study of MAO</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Family‐based case–control study of MAOA and MAOB polymorphisms in Parkinson disease</title></titleInfo><name type="personal"><namePart type="given">Sun J.</namePart><namePart type="family">Kang</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><affiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">William K.</namePart><namePart type="family">Scott</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><affiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yi‐Ju</namePart><namePart type="family">Li</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><affiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael A.</namePart><namePart type="family">Hauser</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><affiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joelle M.</namePart><namePart type="family">van der Walt</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><affiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kenichiro</namePart><namePart type="family">Fujiwara</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregory M.</namePart><namePart type="family">Mayhew</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sandra G.</namePart><namePart type="family">West</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeffery M.</namePart><namePart type="family">Vance</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><affiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eden R.</namePart><namePart type="family">Martin</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Human Genetics, Duke University Medical Center, Durham, North Carolina, USA</affiliation><affiliation>Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA</affiliation><description>Correspondence: Center for Human Genetics, Duke University Medical Center, DUMC, Box 3445, Durham, NC 27710</description><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">2006-12</dateIssued><dateCaptured encoding="w3cdtf">2006-03-16</dateCaptured><dateValid encoding="w3cdtf">2006-07-05</dateValid><copyrightDate encoding="w3cdtf">2006</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">4</extent><extent unit="references">22</extent><extent unit="words">4244</extent></physicalDescription><abstract lang="en">Monoamine oxidase (MAO) is an enzyme regulating metabolism of neurotransmitters such as dopamine. Two distinct forms of enzyme, encoded by genes MAOA and MAOB located on the X chromosome, have been considered as possible factors in the pathogenesis of Parkinson disease (PD). Previous association studies of PD and MAO genes reported inconsistent results. In this study, we used a large family‐based data set to test associations between MAO genes and a risk of PD. The data set includes 298 female discordant sibpairs and 348 male discordant sibpairs. For this study, all subjects analyzed were white and families with known parkin mutations were removed. We analyzed 15 single nucleotide polymorphisms (SNPs) and a dinucleotide repeat marker in the MAO genes. Association was found with the intron 13 SNP of MAOB in the female subset (P = 0.02). No significant association was found in the male subset. Our results add to the evidence of involvement of MAOB in PD and suggest that the effect may be stronger in women. © 2006 Movement Disorder Society</abstract><note type="funding">National Institutes of Health - No. NS39764; No. NS051355; </note><subject lang="en"><genre>Keywords</genre><topic>PD</topic><topic>MAOA</topic><topic>MAOB</topic><topic>family‐based association</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>2175</start><end>2180</end><total>6</total></extent></part></relatedItem><identifier type="istex">F5A10EB001E33C6DB921F3F2610F89C2719BEF62</identifier><identifier type="DOI">10.1002/mds.21151</identifier><identifier type="ArticleID">MDS21151</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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