Coffee, caffeine‐related genes, and Parkinson's disease: A case–control study
Identifieur interne : 001340 ( Istex/Corpus ); précédent : 001339; suivant : 001341Coffee, caffeine‐related genes, and Parkinson's disease: A case–control study
Auteurs : Maurizio F. Facheris ; Nicole K. Schneider ; Timothy G. Lesnick ; Mariza De Andrade ; Julie M. Cunningham ; Walter A. Rocca ; Demetrius M. MaraganoreSource :
- Movement Disorders [ 0885-3185 ] ; 2008-10-30.
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Abstract
An inverse association between coffee and Parkinson's disease (PD) has been reported. However, it remains uncertain why some but not all coffee drinkers are less susceptible to PD. We considered the possibility of a pharmacogenetic effect. In our study, we included 1,208 subjects (446 case‐unaffected sibling pairs and 158 case‐unrelated control pairs) recruited from an ongoing study of the molecular epidemiology of PD in the Upper Midwest (USA). We collected information on lifetime coffee drinking and we studied two genes: ADORA2A, which encodes the major receptor activity of caffeine in the brain (variants rs5751876 and rs3032740), and CYP1A2, which encodes the major rate‐limiting step of caffeine metabolism (variants rs35694136 and rs762551). We did not observe significant associations of coffee drinking or of the genetic variants with PD susceptibility, either independently or jointly, in the sample overall and in most strata. Our study neither supports the hypothesis that coffee protects against PD nor provides evidence for a pharmacogenetic effect. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.22247
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However, it remains uncertain why some but not all coffee drinkers are less susceptible to PD. We considered the possibility of a pharmacogenetic effect. In our study, we included 1,208 subjects (446 case‐unaffected sibling pairs and 158 case‐unrelated control pairs) recruited from an ongoing study of the molecular epidemiology of PD in the Upper Midwest (USA). We collected information on lifetime coffee drinking and we studied two genes: ADORA2A, which encodes the major receptor activity of caffeine in the brain (variants rs5751876 and rs3032740), and CYP1A2, which encodes the major rate‐limiting step of caffeine metabolism (variants rs35694136 and rs762551). We did not observe significant associations of coffee drinking or of the genetic variants with PD susceptibility, either independently or jointly, in the sample overall and in most strata. Our study neither supports the hypothesis that coffee protects against PD nor provides evidence for a pharmacogenetic effect. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Maurizio F. Facheris MD, MSc</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Nicole K. Schneider BA</name><affiliations><json:string>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Timothy G. Lesnick MS</name><affiliations><json:string>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Mariza de Andrade PhD</name><affiliations><json:string>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Julie M. Cunningham PhD</name><affiliations><json:string>Department of Laboratory Medicine, Mayo Clinic, Rochester, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Walter A. Rocca MD, MPH</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA</json:string><json:string>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Demetrius M. 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We collected information on lifetime coffee drinking and we studied two genes: ADORA2A, which encodes the major receptor activity of caffeine in the brain (variants rs5751876 and rs3032740), and CYP1A2, which encodes the major rate‐limiting step of caffeine metabolism (variants rs35694136 and rs762551). We did not observe significant associations of coffee drinking or of the genetic variants with PD susceptibility, either independently or jointly, in the sample overall and in most strata. 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We considered the possibility of a pharmacogenetic effect. In our study, we included 1,208 subjects (446 case‐unaffected sibling pairs and 158 case‐unrelated control pairs) recruited from an ongoing study of the molecular epidemiology of PD in the Upper Midwest (USA). We collected information on lifetime coffee drinking and we studied two genes: ADORA2A, which encodes the major receptor activity of caffeine in the brain (variants rs5751876 and rs3032740), and CYP1A2, which encodes the major rate‐limiting step of caffeine metabolism (variants rs35694136 and rs762551). We did not observe significant associations of coffee drinking or of the genetic variants with PD susceptibility, either independently or jointly, in the sample overall and in most strata. Our study neither supports the hypothesis that coffee protects against PD nor provides evidence for a pharmacogenetic effect. © 2008 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>coffee</term></item><item><term>genes</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="2008-01-20">Received</change><change when="2008-07-01">Registration</change><change when="2008-10-30">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/59393BEDCB3F50FE8F4A5DCF1542AC8DCAF61CBA/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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M.</givenNames><familyName>Maraganore</familyName><degrees>MD</degrees></personName><contactDetails><email>dmaraganore@mayo.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Laboratory Medicine, Mayo Clinic, Rochester, Minnesota, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">coffee</keyword><keyword xml:id="kwd3">genes</keyword></keywordGroup><fundingInfo><fundingAgency>National Institutes of Health</fundingAgency><fundingNumber>NS 33978</fundingNumber><fundingNumber>ES 10751</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>An inverse association between coffee and Parkinson's disease (PD) has been reported. However, it remains uncertain why some but not all coffee drinkers are less susceptible to PD. We considered the possibility of a pharmacogenetic effect. In our study, we included 1,208 subjects (446 case‐unaffected sibling pairs and 158 case‐unrelated control pairs) recruited from an ongoing study of the molecular epidemiology of PD in the Upper Midwest (USA). We collected information on lifetime coffee drinking and we studied two genes: <i>ADORA2A</i>, which encodes the major receptor activity of caffeine in the brain (variants rs5751876 and rs3032740), and <i>CYP1A2</i>, which encodes the major rate‐limiting step of caffeine metabolism (variants rs35694136 and rs762551). We did not observe significant associations of coffee drinking or of the genetic variants with PD susceptibility, either independently or jointly, in the sample overall and in most strata. Our study neither supports the hypothesis that coffee protects against PD nor provides evidence for a pharmacogenetic effect. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn10"><p>Potential conflict of interest: None reported.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Coffee, caffeine‐related genes, and Parkinson's disease: A case–control study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Coffee, Genes, and Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Coffee, caffeine‐related genes, and Parkinson's disease: A case–control study</title></titleInfo><name type="personal"><namePart type="given">Maurizio F.</namePart><namePart type="family">Facheris</namePart><namePart type="termsOfAddress">MD, MSc</namePart><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nicole K.</namePart><namePart type="family">Schneider</namePart><namePart type="termsOfAddress">BA</namePart><affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Timothy G.</namePart><namePart type="family">Lesnick</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mariza</namePart><namePart type="family">de Andrade</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Julie M.</namePart><namePart type="family">Cunningham</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Laboratory Medicine, Mayo Clinic, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Walter A.</namePart><namePart type="family">Rocca</namePart><namePart type="termsOfAddress">MD, MPH</namePart><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA</affiliation><affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Demetrius M.</namePart><namePart type="family">Maraganore</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA</affiliation><description>Correspondence: Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2008-10-30</dateIssued><dateCaptured encoding="w3cdtf">2008-01-20</dateCaptured><dateValid encoding="w3cdtf">2008-07-01</dateValid><copyrightDate encoding="w3cdtf">2008</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">40</extent><extent unit="words">6449</extent></physicalDescription><abstract lang="en">An inverse association between coffee and Parkinson's disease (PD) has been reported. However, it remains uncertain why some but not all coffee drinkers are less susceptible to PD. We considered the possibility of a pharmacogenetic effect. In our study, we included 1,208 subjects (446 case‐unaffected sibling pairs and 158 case‐unrelated control pairs) recruited from an ongoing study of the molecular epidemiology of PD in the Upper Midwest (USA). We collected information on lifetime coffee drinking and we studied two genes: ADORA2A, which encodes the major receptor activity of caffeine in the brain (variants rs5751876 and rs3032740), and CYP1A2, which encodes the major rate‐limiting step of caffeine metabolism (variants rs35694136 and rs762551). We did not observe significant associations of coffee drinking or of the genetic variants with PD susceptibility, either independently or jointly, in the sample overall and in most strata. Our study neither supports the hypothesis that coffee protects against PD nor provides evidence for a pharmacogenetic effect. © 2008 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">National Institutes of Health - No. NS 33978; No. ES 10751; </note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>coffee</topic><topic>genes</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><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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>14</number></detail><extent unit="pages"><start>2033</start><end>2040</end><total>8</total></extent></part></relatedItem><identifier type="istex">59393BEDCB3F50FE8F4A5DCF1542AC8DCAF61CBA</identifier><identifier type="DOI">10.1002/mds.22247</identifier><identifier type="ArticleID">MDS22247</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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