Lack of effect of polymorphisms in dopamine metabolism related genes on imaging of TRODAT‐1 in striatum of asymptomatic volunteers and patients with Parkinson's disease
Identifieur interne : 000855 ( Istex/Corpus ); précédent : 000854; suivant : 000856Lack of effect of polymorphisms in dopamine metabolism related genes on imaging of TRODAT‐1 in striatum of asymptomatic volunteers and patients with Parkinson's disease
Auteurs : David R. Lynch ; P. David Mozley ; Set Sokol ; Nicole M. C. Maas ; Laura J. Balcer ; Andrew D. SiderowfSource :
- Movement Disorders [ 0885-3185 ] ; 2003-07.
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- KwdEn :
Abstract
SPECT scanning using 99Tc‐TRODAT‐1, a ligand that binds to dopamine transporters, may be useful for detection of early Parkinson's disease (PD), diagnosis of presymptomatic individuals, and monitoring disease progression. Understanding whether genetic factors contribute to inter‐individual variability is crucial for interpreting imaging results in the context of disease pathophysiology. We tested whether polymorphisms in the genes for catechol‐O‐methyltransferase (COMT), monoamine‐oxidase B (MAO‐B), and the dopamine transporter (DAT) influence dopamine uptake parameters in the striatum in vivo in asymptomatic volunteers and patients with PD as measured with 99Tc‐TRODAT‐1. 99Tc‐TRODAT‐1 binding declined with age in both asymptomatic volunteers and PD patients, and depended on disease duration in PD patients. We found no significant association between COMT, MAO‐B, and DAT polymorphisms and results of 99Tc‐TRODAT‐1 testing in asymptomatic volunteers or patients with PD. In PD patients, the age of disease onset and speed of progression did not differ based on these polymorphisms. These results demonstrate that these specific genetic variations do not alter the fidelity of 99Tc‐TRODAT‐1 as a measure of dopaminergic function in asymptomatic volunteer individuals or patients with PD. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10430
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ISTEX:117E05FDD932CE8C1DB40D09EEDAA0FAF3E58653Le document en format XML
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Understanding whether genetic factors contribute to inter‐individual variability is crucial for interpreting imaging results in the context of disease pathophysiology. We tested whether polymorphisms in the genes for catechol‐O‐methyltransferase (COMT), monoamine‐oxidase B (MAO‐B), and the dopamine transporter (DAT) influence dopamine uptake parameters in the striatum in vivo in asymptomatic volunteers and patients with PD as measured with 99Tc‐TRODAT‐1. 99Tc‐TRODAT‐1 binding declined with age in both asymptomatic volunteers and PD patients, and depended on disease duration in PD patients. We found no significant association between COMT, MAO‐B, and DAT polymorphisms and results of 99Tc‐TRODAT‐1 testing in asymptomatic volunteers or patients with PD. In PD patients, the age of disease onset and speed of progression did not differ based on these polymorphisms. These results demonstrate that these specific genetic variations do not alter the fidelity of 99Tc‐TRODAT‐1 as a measure of dopaminergic function in asymptomatic volunteer individuals or patients with PD. © 2003 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>David R. Lynch MD, PhD</name><affiliations><json:string>Department of Neurology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</json:string><json:string>Department of Pediatrics, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</json:string></affiliations></json:item><json:item><name>P. 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Understanding whether genetic factors contribute to inter‐individual variability is crucial for interpreting imaging results in the context of disease pathophysiology. We tested whether polymorphisms in the genes for catechol‐O‐methyltransferase (COMT), monoamine‐oxidase B (MAO‐B), and the dopamine transporter (DAT) influence dopamine uptake parameters in the striatum in vivo in asymptomatic volunteers and patients with PD as measured with 99Tc‐TRODAT‐1. 99Tc‐TRODAT‐1 binding declined with age in both asymptomatic volunteers and PD patients, and depended on disease duration in PD patients. We found no significant association between COMT, MAO‐B, and DAT polymorphisms and results of 99Tc‐TRODAT‐1 testing in asymptomatic volunteers or patients with PD. In PD patients, the age of disease onset and speed of progression did not differ based on these polymorphisms. 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These results demonstrate that these specific genetic variations do not alter the fidelity of 99Tc‐TRODAT‐1 as a measure of dopaminergic function in asymptomatic volunteer individuals or patients with PD. © 2003 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>parkinsonism</term></item><item><term>PET</term></item><item><term>polymorphism</term></item><item><term>genetic risk</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="2002-05-09">Received</change><change when="2002-11-23">Registration</change><change when="2003-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/117E05FDD932CE8C1DB40D09EEDAA0FAF3E58653/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="short">Mov. 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Understanding whether genetic factors contribute to inter‐individual variability is crucial for interpreting imaging results in the context of disease pathophysiology. We tested whether polymorphisms in the genes for catechol‐<i>O</i>‐methyltransferase (COMT), monoamine‐oxidase B (MAO‐B), and the dopamine transporter (DAT) influence dopamine uptake parameters in the striatum in vivo in asymptomatic volunteers and patients with PD as measured with <sup>99</sup>Tc‐TRODAT‐1. <sup>99</sup>Tc‐TRODAT‐1 binding declined with age in both asymptomatic volunteers and PD patients, and depended on disease duration in PD patients. We found no significant association between COMT, MAO‐B, and DAT polymorphisms and results of <sup>99</sup>Tc‐TRODAT‐1 testing in asymptomatic volunteers or patients with PD. In PD patients, the age of disease onset and speed of progression did not differ based on these polymorphisms. These results demonstrate that these specific genetic variations do not alter the fidelity of <sup>99</sup>Tc‐TRODAT‐1 as a measure of dopaminergic function in asymptomatic volunteer individuals or patients with PD. © 2003 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Lack of effect of polymorphisms in dopamine metabolism related genes on imaging of TRODAT‐1 in striatum of asymptomatic volunteers and patients with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Polymorphisms in TRODAT‐1 Spect in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Lack of effect of polymorphisms in dopamine metabolism related genes on imaging of TRODAT‐1 in striatum of asymptomatic volunteers and patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">David R.</namePart><namePart type="family">Lynch</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</affiliation><affiliation>Department of Pediatrics, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</affiliation><description>Correspondence: Division of Neurology, Children's Hospital of Philadelphia, 502 Abramson Building, Philadelphia, PA 19104‐4318</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P. David</namePart><namePart type="family">Mozley</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Radiology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Set</namePart><namePart type="family">Sokol</namePart><namePart type="termsOfAddress">BA</namePart><affiliation>Department of Neurology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nicole M.C.</namePart><namePart type="family">Maas</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pediatrics, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laura J.</namePart><namePart type="family">Balcer</namePart><namePart type="termsOfAddress">MD, MSCE</namePart><affiliation>Department of Neurology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew D.</namePart><namePart type="family">Siderowf</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA</affiliation><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">2003-07</dateIssued><dateCaptured encoding="w3cdtf">2002-05-09</dateCaptured><dateValid encoding="w3cdtf">2002-11-23</dateValid><copyrightDate encoding="w3cdtf">2003</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">2</extent><extent unit="tables">5</extent><extent unit="references">24</extent><extent unit="words">4969</extent></physicalDescription><abstract lang="en">SPECT scanning using 99Tc‐TRODAT‐1, a ligand that binds to dopamine transporters, may be useful for detection of early Parkinson's disease (PD), diagnosis of presymptomatic individuals, and monitoring disease progression. Understanding whether genetic factors contribute to inter‐individual variability is crucial for interpreting imaging results in the context of disease pathophysiology. We tested whether polymorphisms in the genes for catechol‐O‐methyltransferase (COMT), monoamine‐oxidase B (MAO‐B), and the dopamine transporter (DAT) influence dopamine uptake parameters in the striatum in vivo in asymptomatic volunteers and patients with PD as measured with 99Tc‐TRODAT‐1. 99Tc‐TRODAT‐1 binding declined with age in both asymptomatic volunteers and PD patients, and depended on disease duration in PD patients. We found no significant association between COMT, MAO‐B, and DAT polymorphisms and results of 99Tc‐TRODAT‐1 testing in asymptomatic volunteers or patients with PD. In PD patients, the age of disease onset and speed of progression did not differ based on these polymorphisms. These results demonstrate that these specific genetic variations do not alter the fidelity of 99Tc‐TRODAT‐1 as a measure of dopaminergic function in asymptomatic volunteer individuals or patients with PD. © 2003 Movement Disorder Society</abstract><note type="funding">National Institutes of Health - No. AG17524; No. EY00351; </note><note type="funding">Beeson Scholar Award</note><note type="funding">Agency for Healthcare Research and Quality - No. HS00004; </note><subject lang="en"><genre>Keywords</genre><topic>parkinsonism</topic><topic>PET</topic><topic>polymorphism</topic><topic>genetic risk</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><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>2003</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>804</start><end>812</end><total>8</total></extent></part></relatedItem><identifier type="istex">117E05FDD932CE8C1DB40D09EEDAA0FAF3E58653</identifier><identifier type="DOI">10.1002/mds.10430</identifier><identifier type="ArticleID">MDS10430</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 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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