Analysis of LRRK2 Gly2385Arg genetic variant in non‐Chinese Asians
Identifieur interne : 001608 ( Main/Corpus ); précédent : 001607; suivant : 001609Analysis of LRRK2 Gly2385Arg genetic variant in non‐Chinese Asians
Auteurs : Eng-King Tan ; Yi Zhao ; Louis Tan ; Hui-Qin Lim ; Jasinda Lee ; Yih Yuen ; Ratnagopal Pavanni ; Meng-Cheong Wong ; Stephanie Fook-Chong ; Jian-Jun LiuSource :
- Movement Disorders [ 0885-3185 ] ; 2007-09-15.
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Abstract
A common LRRK2 missense variant, Gly2385Arg, has been found to be a genetic risk factor for Parkinson's disease (PD) in ethnic Chinese and Japanese. However, the presence of the variant in other non‐Chinese Asian patients has not been fully clarified. We performed genetic analysis of the Gly2385Arg variant in 472 non‐Chinese Asian subjects in Singapore (comprising of 166 PD and 306 controls of Malay/Indian ethnicity). The frequency of the heterozygous Gly2385Arg genotype was not significantly different in PD compared with controls (1.2% vs. 0.8%, odds ratio = 2.83, 95% CI 0.40, 20.2, P = 0.3). No subjects carried the homozygous genotype. Stratification by Malay and Indian ethnicity revealed that there were two carriers each among 98 (2.0%) Malay PD and 173 (1.2%) Malay controls (odds ratio = 1.78, 95% CI 0.25, 12.8, P = 0.6), but there were no carriers among 66 Indian PD and 133 Indian controls. We demonstrated that the Gly2385Arg variant could be detected in our Malay subjects. However, its frequency was much lower than the 8 to 10% prevalence previously reported in our Singaporean and Taiwanese Chinese PD population. The relevance of Gly2385Arg as a genetic risk factor may be restricted to selected Asian races, and more studies will be needed to confirm our observations. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21658
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-09-15">2007-09-15</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1816">1816</biblScope><biblScope unit="page" to="1818">1818</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">0F32308AC7F48A3E60B1581A9E0D79C25A8533BE</idno><idno type="DOI">10.1002/mds.21658</idno><idno type="ArticleID">MDS21658</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>LRRK2</term><term>Parkinson's disease</term><term>mutation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A common LRRK2 missense variant, Gly2385Arg, has been found to be a genetic risk factor for Parkinson's disease (PD) in ethnic Chinese and Japanese. However, the presence of the variant in other non‐Chinese Asian patients has not been fully clarified. We performed genetic analysis of the Gly2385Arg variant in 472 non‐Chinese Asian subjects in Singapore (comprising of 166 PD and 306 controls of Malay/Indian ethnicity). The frequency of the heterozygous Gly2385Arg genotype was not significantly different in PD compared with controls (1.2% vs. 0.8%, odds ratio = 2.83, 95% CI 0.40, 20.2, P = 0.3). No subjects carried the homozygous genotype. Stratification by Malay and Indian ethnicity revealed that there were two carriers each among 98 (2.0%) Malay PD and 173 (1.2%) Malay controls (odds ratio = 1.78, 95% CI 0.25, 12.8, P = 0.6), but there were no carriers among 66 Indian PD and 133 Indian controls. We demonstrated that the Gly2385Arg variant could be detected in our Malay subjects. However, its frequency was much lower than the 8 to 10% prevalence previously reported in our Singaporean and Taiwanese Chinese PD population. The relevance of Gly2385Arg as a genetic risk factor may be restricted to selected Asian races, and more studies will be needed to confirm our observations. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Eng‐King Tan MD</name><affiliations><json:string>Department of Neurology, Singapore General Hospital, Singapore</json:string><json:string>Department of Neurology, National Neuroscience Institute, Singapore</json:string><json:string>SingHealth Research, Singapore</json:string></affiliations></json:item><json:item><name>Yi Zhao MD, PhD</name><affiliations><json:string>Department of Clinical Research, Singapore General Hospital, Singapore</json:string></affiliations></json:item><json:item><name>Louis Tan MD</name><affiliations><json:string>Department of Neurology, National Neuroscience Institute, Singapore</json:string></affiliations></json:item><json:item><name>Hui‐Qin Lim BSc</name><affiliations><json:string>Department of Neurology, Singapore General Hospital, Singapore</json:string></affiliations></json:item><json:item><name>Jasinda Lee BSc</name><affiliations><json:string>Department of Neurology, Singapore General Hospital, Singapore</json:string></affiliations></json:item><json:item><name>Yih Yuen MD</name><affiliations><json:string>Department of Health Screening, Singapore General Hospital, Singapore</json:string></affiliations></json:item><json:item><name>Ratnagopal Pavanni MD</name><affiliations><json:string>Department of Neurology, Singapore General Hospital, Singapore</json:string><json:string>SingHealth Research, Singapore</json:string></affiliations></json:item><json:item><name>Meng‐Cheong Wong MD</name><affiliations><json:string>Department of Neurology, Singapore General Hospital, Singapore</json:string><json:string>SingHealth Research, Singapore</json:string></affiliations></json:item><json:item><name>Stephanie Fook‐Chong MSc</name><affiliations><json:string>Department of Clinical Research, Singapore General Hospital, Singapore</json:string></affiliations></json:item><json:item><name>Jian‐Jun Liu PhD</name><affiliations><json:string>Population Genetics, Genome Institute of Singapore, Singapore</json:string></affiliations></json:item></author><subject><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>LRRK2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mutation</value></json:item></subject><articleId><json:string>MDS21658</json:string></articleId><language><json:string>eng</json:string></language><abstract>A common LRRK2 missense variant, Gly2385Arg, has been found to be a genetic risk factor for Parkinson's disease (PD) in ethnic Chinese and Japanese. However, the presence of the variant in other non‐Chinese Asian patients has not been fully clarified. We performed genetic analysis of the Gly2385Arg variant in 472 non‐Chinese Asian subjects in Singapore (comprising of 166 PD and 306 controls of Malay/Indian ethnicity). The frequency of the heterozygous Gly2385Arg genotype was not significantly different in PD compared with controls (1.2% vs. 0.8%, odds ratio = 2.83, 95% CI 0.40, 20.2, P = 0.3). No subjects carried the homozygous genotype. Stratification by Malay and Indian ethnicity revealed that there were two carriers each among 98 (2.0%) Malay PD and 173 (1.2%) Malay controls (odds ratio = 1.78, 95% CI 0.25, 12.8, P = 0.6), but there were no carriers among 66 Indian PD and 133 Indian controls. We demonstrated that the Gly2385Arg variant could be detected in our Malay subjects. However, its frequency was much lower than the 8 to 10% prevalence previously reported in our Singaporean and Taiwanese Chinese PD population. The relevance of Gly2385Arg as a genetic risk factor may be restricted to selected Asian races, and more studies will be needed to confirm our observations. © 2007 Movement Disorder Society</abstract><qualityIndicators><score>4.749</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1326</abstractCharCount><pdfWordCount>2181</pdfWordCount><pdfCharCount>13532</pdfCharCount><pdfPageCount>3</pdfPageCount><abstractWordCount>214</abstractWordCount></qualityIndicators><title>Analysis of LRRK2 Gly2385Arg genetic variant in non‐Chinese Asians</title><genre><json:string>article</json:string></genre><host><volume>22</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>3</total><last>1818</last><first>1816</first></pages><issn><json:string>0885-3185</json:string></issn><issue>12</issue><subject><json:item><value>Brief 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Department of Neurology, Singapore General Hospital, National Neuroscience Institute, SingHealth, Outram Road, Singapore 169608</p></note><affiliation>Department of Neurology, Singapore General Hospital, Singapore</affiliation><affiliation>Department of Neurology, National Neuroscience Institute, Singapore</affiliation><affiliation>SingHealth Research, Singapore</affiliation></author><author><persName><forename type="first">Yi</forename><surname>Zhao</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Clinical Research, Singapore General Hospital, Singapore</affiliation></author><author><persName><forename type="first">Louis</forename><surname>Tan</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, National Neuroscience Institute, Singapore</affiliation></author><author><persName><forename type="first">Hui‐Qin</forename><surname>Lim</surname></persName><roleName 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However, the presence of the variant in other non‐Chinese Asian patients has not been fully clarified. We performed genetic analysis of the Gly2385Arg variant in 472 non‐Chinese Asian subjects in Singapore (comprising of 166 PD and 306 controls of Malay/Indian ethnicity). The frequency of the heterozygous Gly2385Arg genotype was not significantly different in PD compared with controls (1.2% vs. 0.8%, odds ratio = 2.83, 95% CI 0.40, 20.2, P = 0.3). No subjects carried the homozygous genotype. Stratification by Malay and Indian ethnicity revealed that there were two carriers each among 98 (2.0%) Malay PD and 173 (1.2%) Malay controls (odds ratio = 1.78, 95% CI 0.25, 12.8, P = 0.6), but there were no carriers among 66 Indian PD and 133 Indian controls. We demonstrated that the Gly2385Arg variant could be detected in our Malay subjects. However, its frequency was much lower than the 8 to 10% prevalence previously reported in our Singaporean and Taiwanese Chinese PD population. The relevance of Gly2385Arg as a genetic risk factor may be restricted to selected Asian races, and more studies will be needed to confirm our observations. © 2007 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>LRRK2</term></item><item><term>mutation</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-01-05">Received</change><change when="2007-06-11">Registration</change><change when="2007-09-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0F32308AC7F48A3E60B1581A9E0D79C25A8533BE/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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type="manuscriptAccepted" date="2007-06-11"></event><event type="publishedOnlineEarlyUnpaginated" date="2007-07-20"></event><event type="firstOnline" date="2007-07-20"></event><event type="publishedOnlineFinalForm" date="2007-09-21"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1816</numbering><numbering type="pageLast">1818</numbering></numberingGroup><correspondenceTo>Department of Neurology, Singapore General Hospital, National Neuroscience Institute, SingHealth, Outram Road, Singapore 169608</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21658.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="24"></count><count type="wordTotal" number="2440"></count></countGroup><titleGroup><title type="main" xml:lang="en">Analysis of <i>LRRK2</i> Gly2385Arg genetic variant in non‐Chinese Asians</title><title type="short" xml:lang="en">LRRK2 Gly2385Arg Variant in Non‐Chinese Asians</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2 #af3" corresponding="yes"><personName><givenNames>Eng‐King</givenNames><familyName>Tan</familyName><degrees>MD</degrees></personName><contactDetails><email>gnrtek@sgh.com.sg</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Yi</givenNames><familyName>Zhao</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Louis</givenNames><familyName>Tan</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hui‐Qin</givenNames><familyName>Lim</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jasinda</givenNames><familyName>Lee</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Yih</givenNames><familyName>Yuen</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Ratnagopal</givenNames><familyName>Pavanni</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Meng‐Cheong</givenNames><familyName>Wong</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Stephanie</givenNames><familyName>Fook‐Chong</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Jian‐Jun</givenNames><familyName>Liu</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="SG" type="organization"><unparsedAffiliation>Department of Neurology, Singapore General Hospital, Singapore</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="SG" type="organization"><unparsedAffiliation>Department of Neurology, National Neuroscience Institute, Singapore</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="SG" type="organization"><unparsedAffiliation>SingHealth Research, Singapore</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="SG" type="organization"><unparsedAffiliation>Department of Clinical Research, Singapore General Hospital, Singapore</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="SG" type="organization"><unparsedAffiliation>Department of Health Screening, Singapore General Hospital, Singapore</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="SG" type="organization"><unparsedAffiliation>Population Genetics, Genome Institute of Singapore, Singapore</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2"><i>LRRK2</i></keyword><keyword xml:id="kwd3">mutation</keyword></keywordGroup><fundingInfo><fundingAgency>National Medical Research Council</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Biomedical Research Council</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Department of Clinical Research, Singapore General Hospital</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>A common <i>LRRK2</i> missense variant, Gly2385Arg, has been found to be a genetic risk factor for Parkinson's disease (PD) in ethnic Chinese and Japanese. However, the presence of the variant in other non‐Chinese Asian patients has not been fully clarified. We performed genetic analysis of the Gly2385Arg variant in 472 non‐Chinese Asian subjects in Singapore (comprising of 166 PD and 306 controls of Malay/Indian ethnicity). The frequency of the heterozygous Gly2385Arg genotype was not significantly different in PD compared with controls (1.2% vs. 0.8%, odds ratio = 2.83, 95% CI 0.40, 20.2, <i>P</i> = 0.3). No subjects carried the homozygous genotype. Stratification by Malay and Indian ethnicity revealed that there were two carriers each among 98 (2.0%) Malay PD and 173 (1.2%) Malay controls (odds ratio = 1.78, 95% CI 0.25, 12.8, <i>P</i> = 0.6), but there were no carriers among 66 Indian PD and 133 Indian controls. We demonstrated that the Gly2385Arg variant could be detected in our Malay subjects. However, its frequency was much lower than the 8 to 10% prevalence previously reported in our Singaporean and Taiwanese Chinese PD population. The relevance of Gly2385Arg as a genetic risk factor may be restricted to selected Asian races, and more studies will be needed to confirm our observations. © 2007 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Analysis of LRRK2 Gly2385Arg genetic variant in non‐Chinese Asians</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>LRRK2 Gly2385Arg Variant in Non‐Chinese Asians</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Analysis of</title></titleInfo><name type="personal"><namePart type="given">Eng‐King</namePart><namePart type="family">Tan</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Singapore General Hospital, Singapore</affiliation><affiliation>Department of Neurology, National Neuroscience Institute, Singapore</affiliation><affiliation>SingHealth Research, Singapore</affiliation><description>Correspondence: Department of Neurology, Singapore General Hospital, National Neuroscience Institute, SingHealth, Outram Road, Singapore 169608</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yi</namePart><namePart type="family">Zhao</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Clinical Research, Singapore General Hospital, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Louis</namePart><namePart type="family">Tan</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, National Neuroscience Institute, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hui‐Qin</namePart><namePart type="family">Lim</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Department of Neurology, Singapore General Hospital, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jasinda</namePart><namePart type="family">Lee</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Department of Neurology, Singapore General Hospital, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yih</namePart><namePart type="family">Yuen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Health Screening, Singapore General Hospital, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ratnagopal</namePart><namePart type="family">Pavanni</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Singapore General Hospital, Singapore</affiliation><affiliation>SingHealth Research, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Meng‐Cheong</namePart><namePart type="family">Wong</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Singapore General Hospital, Singapore</affiliation><affiliation>SingHealth Research, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephanie</namePart><namePart type="family">Fook‐Chong</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Department of Clinical Research, Singapore General Hospital, Singapore</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jian‐Jun</namePart><namePart type="family">Liu</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Population Genetics, Genome Institute of Singapore, Singapore</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">2007-09-15</dateIssued><dateCaptured encoding="w3cdtf">2007-01-05</dateCaptured><dateValid encoding="w3cdtf">2007-06-11</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="tables">1</extent><extent unit="references">24</extent><extent unit="words">2440</extent></physicalDescription><abstract lang="en">A common LRRK2 missense variant, Gly2385Arg, has been found to be a genetic risk factor for Parkinson's disease (PD) in ethnic Chinese and Japanese. However, the presence of the variant in other non‐Chinese Asian patients has not been fully clarified. We performed genetic analysis of the Gly2385Arg variant in 472 non‐Chinese Asian subjects in Singapore (comprising of 166 PD and 306 controls of Malay/Indian ethnicity). The frequency of the heterozygous Gly2385Arg genotype was not significantly different in PD compared with controls (1.2% vs. 0.8%, odds ratio = 2.83, 95% CI 0.40, 20.2, P = 0.3). No subjects carried the homozygous genotype. Stratification by Malay and Indian ethnicity revealed that there were two carriers each among 98 (2.0%) Malay PD and 173 (1.2%) Malay controls (odds ratio = 1.78, 95% CI 0.25, 12.8, P = 0.6), but there were no carriers among 66 Indian PD and 133 Indian controls. We demonstrated that the Gly2385Arg variant could be detected in our Malay subjects. However, its frequency was much lower than the 8 to 10% prevalence previously reported in our Singaporean and Taiwanese Chinese PD population. The relevance of Gly2385Arg as a genetic risk factor may be restricted to selected Asian races, and more studies will be needed to confirm our observations. © 2007 Movement Disorder Society</abstract><note type="funding">National Medical Research Council</note><note type="funding">Biomedical Research Council</note><note type="funding">Department of Clinical Research, Singapore General Hospital</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>LRRK2</topic><topic>mutation</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>Brief Report</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>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>1816</start><end>1818</end><total>3</total></extent></part></relatedItem><identifier type="istex">0F32308AC7F48A3E60B1581A9E0D79C25A8533BE</identifier><identifier type="DOI">10.1002/mds.21658</identifier><identifier type="ArticleID">MDS21658</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 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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