Dopamine turnover increases in asymptomatic LRRK2 mutations carriers
Identifieur interne : 001001 ( Main/Corpus ); précédent : 001000; suivant : 001002Dopamine turnover increases in asymptomatic LRRK2 mutations carriers
Auteurs : Vesna Sossi ; Raul De La Fuente-Fernández ; Ramachandiran Nandhagopal ; Michael Schulzer ; Jessamyn Mckenzie ; Thomas J. Ruth ; Jan O. Aasly ; Matthew J. Farrer ; Zbigniew K. Wszolek ; Jon A. StoesslSource :
- Movement Disorders [ 0885-3185 ] ; 2010-12-15.
English descriptors
Abstract
Increase in dopamine (DA) turnover was found to occur early in symptomatic Parkinson's disease (PD) and to be functionally related to the dopamine transporter (DAT). The objectives of this study were to examine changes in DA turnover in the asymptomatic PD phase; to compare them with changes in other dopaminergic markers, and to investigate a possible relationship between DAT and DA turnover. Eight subjects from families at increased risk of PD due to LRRK2 mutation were investigated. Positron emission tomography imaging was performed with: 18F‐fluorodopa to determine the effective DA distribution volume (EDV), the inverse of DA turnover, and the DA uptake rate Kocc, a marker of DA synthesis and storage; 11C‐methylphenidate (MP, a DAT marker) and 11C‐dihydrotetrabenazine (DTBZ, a VMAT2 marker) to estimate the binding potentials BPND_MP and BPND_DTBZ. On average, EDV showed the largest reduction from age‐matched control values (42%) followed by BPND _ MP (23%) and BPND _ DTBZ (17%), whereas Kocc remained in the normal range for all subjects. No correlation was found between EDV and any other marker. DA turnover was found to be elevated in asymptomatic mutation carriers at increased risk of PD. Such change was determined to be larger than and statistically independent from changes observed with the other markers. These results support a compensatory role of increased DA turnover in presymptomatic disease and indicate that at this stage, in contrast to the symptomatic PD phase, increased turnover is not related to DAT. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23356
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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="2010-12-15">2010-12-15</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">16</biblScope><biblScope unit="page" from="2717">2717</biblScope><biblScope unit="page" to="2723">2723</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">2B49F1CFDF50DF88AA35CE307095DB569960BC13</idno><idno type="DOI">10.1002/mds.23356</idno><idno type="ArticleID">MDS23356</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>LRRK2 mutation</term><term>PET imaging</term><term>Parkinson's disease</term><term>dopamine turnover</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Increase in dopamine (DA) turnover was found to occur early in symptomatic Parkinson's disease (PD) and to be functionally related to the dopamine transporter (DAT). The objectives of this study were to examine changes in DA turnover in the asymptomatic PD phase; to compare them with changes in other dopaminergic markers, and to investigate a possible relationship between DAT and DA turnover. Eight subjects from families at increased risk of PD due to LRRK2 mutation were investigated. Positron emission tomography imaging was performed with: 18F‐fluorodopa to determine the effective DA distribution volume (EDV), the inverse of DA turnover, and the DA uptake rate Kocc, a marker of DA synthesis and storage; 11C‐methylphenidate (MP, a DAT marker) and 11C‐dihydrotetrabenazine (DTBZ, a VMAT2 marker) to estimate the binding potentials BPND_MP and BPND_DTBZ. On average, EDV showed the largest reduction from age‐matched control values (42%) followed by BPND _ MP (23%) and BPND _ DTBZ (17%), whereas Kocc remained in the normal range for all subjects. No correlation was found between EDV and any other marker. DA turnover was found to be elevated in asymptomatic mutation carriers at increased risk of PD. Such change was determined to be larger than and statistically independent from changes observed with the other markers. These results support a compensatory role of increased DA turnover in presymptomatic disease and indicate that at this stage, in contrast to the symptomatic PD phase, increased turnover is not related to DAT. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Vesna Sossi PhD</name><affiliations><json:string>Department of Physics and Astronomy, University of British Columbia, Vancouver British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Raul de la Fuente‐Fernández</name><affiliations><json:string>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Ramachandiran Nandhagopal DM</name><affiliations><json:string>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Michael Schulzer MD, PhD</name><affiliations><json:string>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Jessamyn McKenzie LPN</name><affiliations><json:string>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Thomas J. Ruth PhD</name><affiliations><json:string>TRIUMF, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Jan O. Aasly</name><affiliations><json:string>Department of Neuroscience and Neurology, NTNU, Trondheim, Norway</json:string></affiliations></json:item><json:item><name>Matthew J. Farrer PhD</name><affiliations><json:string>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA</json:string></affiliations></json:item><json:item><name>Zbigniew K. Wszolek MD</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA</json:string></affiliations></json:item><json:item><name>Jon A. 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The objectives of this study were to examine changes in DA turnover in the asymptomatic PD phase; to compare them with changes in other dopaminergic markers, and to investigate a possible relationship between DAT and DA turnover. Eight subjects from families at increased risk of PD due to LRRK2 mutation were investigated. Positron emission tomography imaging was performed with: 18F‐fluorodopa to determine the effective DA distribution volume (EDV), the inverse of DA turnover, and the DA uptake rate Kocc, a marker of DA synthesis and storage; 11C‐methylphenidate (MP, a DAT marker) and 11C‐dihydrotetrabenazine (DTBZ, a VMAT2 marker) to estimate the binding potentials BPND_MP and BPND_DTBZ. On average, EDV showed the largest reduction from age‐matched control values (42%) followed by BPND _ MP (23%) and BPND _ DTBZ (17%), whereas Kocc remained in the normal range for all subjects. No correlation was found between EDV and any other marker. DA turnover was found to be elevated in asymptomatic mutation carriers at increased risk of PD. Such change was determined to be larger than and statistically independent from changes observed with the other markers. These results support a compensatory role of increased DA turnover in presymptomatic disease and indicate that at this stage, in contrast to the symptomatic PD phase, increased turnover is not related to DAT. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>7.23</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1574</abstractCharCount><pdfWordCount>4290</pdfWordCount><pdfCharCount>27196</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>245</abstractWordCount></qualityIndicators><title>Dopamine turnover increases in asymptomatic LRRK2 mutations 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V6T2B5</p></note><affiliation>Department of Physics and Astronomy, University of British Columbia, Vancouver British Columbia, Canada</affiliation></author><author><persName><forename type="first">Raul</forename><surname>de la Fuente‐Fernández</surname></persName><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation></author><author><persName><forename type="first">Ramachandiran</forename><surname>Nandhagopal</surname></persName><roleName type="degree">DM</roleName><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation></author><author><persName><forename type="first">Michael</forename><surname>Schulzer</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation></author><author><persName><forename type="first">Jessamyn</forename><surname>McKenzie</surname></persName><roleName type="degree">LPN</roleName><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation></author><author><persName><forename type="first">Thomas J.</forename><surname>Ruth</surname></persName><roleName type="degree">PhD</roleName><affiliation>TRIUMF, Vancouver, British Columbia, Canada</affiliation></author><author><persName><forename type="first">Jan O.</forename><surname>Aasly</surname></persName><affiliation>Department of Neuroscience and Neurology, NTNU, Trondheim, Norway</affiliation></author><author><persName><forename type="first">Matthew J.</forename><surname>Farrer</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA</affiliation></author><author><persName><forename type="first">Zbigniew K.</forename><surname>Wszolek</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA</affiliation></author><author><persName><forename type="first">Jon A.</forename><surname>Stoessl</surname></persName><roleName type="degree">MD, FRCPC</roleName><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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The objectives of this study were to examine changes in DA turnover in the asymptomatic PD phase; to compare them with changes in other dopaminergic markers, and to investigate a possible relationship between DAT and DA turnover. Eight subjects from families at increased risk of PD due to LRRK2 mutation were investigated. Positron emission tomography imaging was performed with: 18F‐fluorodopa to determine the effective DA distribution volume (EDV), the inverse of DA turnover, and the DA uptake rate Kocc, a marker of DA synthesis and storage; 11C‐methylphenidate (MP, a DAT marker) and 11C‐dihydrotetrabenazine (DTBZ, a VMAT2 marker) to estimate the binding potentials BPND_MP and BPND_DTBZ. On average, EDV showed the largest reduction from age‐matched control values (42%) followed by BPND _ MP (23%) and BPND _ DTBZ (17%), whereas Kocc remained in the normal range for all subjects. No correlation was found between EDV and any other marker. DA turnover was found to be elevated in asymptomatic mutation carriers at increased risk of PD. Such change was determined to be larger than and statistically independent from changes observed with the other markers. These results support a compensatory role of increased DA turnover in presymptomatic disease and indicate that at this stage, in contrast to the symptomatic PD phase, increased turnover is not related to DAT. © 2010 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 mutation</term></item><item><term>PET imaging</term></item><item><term>dopamine turnover</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="2009-09-21">Received</change><change when="2010-05-10">Registration</change><change when="2010-12-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/2B49F1CFDF50DF88AA35CE307095DB569960BC13/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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href="file:MDS.MDS23356.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="38"></count><count type="wordTotal" number="5320"></count></countGroup><titleGroup><title type="main" xml:lang="en">Dopamine turnover increases in asymptomatic <i>LRRK2</i> mutations carriers<link href="#fn10"></link></title><title type="short" xml:lang="en">Dopamine Turnover in Asymptomatic LRRK2</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Vesna</givenNames><familyName>Sossi</familyName><degrees>PhD</degrees></personName><contactDetails><email>vesna@phas.ubc.ca</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Raul</givenNames><familyName>de la Fuente‐Fernández</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Ramachandiran</givenNames><familyName>Nandhagopal</familyName><degrees>DM</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Michael</givenNames><familyName>Schulzer</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Jessamyn</givenNames><familyName>McKenzie</familyName><degrees>LPN</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Thomas J.</givenNames><familyName>Ruth</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Jan O.</givenNames><familyName>Aasly</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Matthew J.</givenNames><familyName>Farrer</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Zbigniew K.</givenNames><familyName>Wszolek</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Jon A.</givenNames><familyName>Stoessl</familyName><degrees>MD, FRCPC</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Department of Physics and Astronomy, University of British Columbia, Vancouver British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>TRIUMF, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="NO" type="organization"><unparsedAffiliation>Department of Neuroscience and Neurology, NTNU, Trondheim, Norway</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">LRRK2 mutation</keyword><keyword xml:id="kwd3">PET imaging</keyword><keyword xml:id="kwd4">dopamine turnover</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Increase in dopamine (DA) turnover was found to occur early in symptomatic Parkinson's disease (PD) and to be functionally related to the dopamine transporter (DAT). The objectives of this study were to examine changes in DA turnover in the asymptomatic PD phase; to compare them with changes in other dopaminergic markers, and to investigate a possible relationship between DAT and DA turnover. Eight subjects from families at increased risk of PD due to <i>LRRK2</i> mutation were investigated. Positron emission tomography imaging was performed with: <sup>18</sup>F‐fluorodopa to determine the effective DA distribution volume (EDV), the inverse of DA turnover, and the DA uptake rate <i>K</i><sub>occ</sub>, a marker of DA synthesis and storage; <sup>11</sup>C‐methylphenidate (MP, a DAT marker) and <sup>11</sup>C‐dihydrotetrabenazine (DTBZ, a VMAT2 marker) to estimate the binding potentials BP<sub>ND_MP</sub> and BP<sub>ND_DTBZ</sub>. On average, EDV showed the largest reduction from age‐matched control values (42%) followed by BP<sub>ND</sub><sub>_</sub><sub>MP</sub> (23%) and BP<sub>ND</sub><sub>_</sub><sub>DTBZ</sub> (17%), whereas <i>K</i><sub>occ</sub> remained in the normal range for all subjects. No correlation was found between EDV and any other marker. DA turnover was found to be elevated in asymptomatic mutation carriers at increased risk of PD. Such change was determined to be larger than and statistically independent from changes observed with the other markers. These results support a compensatory role of increased DA turnover in presymptomatic disease and indicate that at this stage, in contrast to the symptomatic PD phase, increased turnover is not related to DAT. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn10"><p>Potential conflict of interest: Authors do not report any conflict of interest or relevant financial interest in this manuscript.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dopamine turnover increases in asymptomatic LRRK2 mutations carriers</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dopamine Turnover in Asymptomatic LRRK2</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Dopamine turnover increases in asymptomatic</title></titleInfo><name type="personal"><namePart type="given">Vesna</namePart><namePart type="family">Sossi</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Physics and Astronomy, University of British Columbia, Vancouver British Columbia, Canada</affiliation><description>Correspondence: Pacific Parkinson's Research Centre, University of British Columbia, Vancouver Hospital and Health Sciences Centre, Purdy Pavilion, 2221 Wesbrook Mall, Vancouver, British Columbia, Canada V6T2B5</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Raul</namePart><namePart type="family">de la Fuente‐Fernández</namePart><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ramachandiran</namePart><namePart type="family">Nandhagopal</namePart><namePart type="termsOfAddress">DM</namePart><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Schulzer</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jessamyn</namePart><namePart type="family">McKenzie</namePart><namePart type="termsOfAddress">LPN</namePart><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas J.</namePart><namePart type="family">Ruth</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>TRIUMF, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan O.</namePart><namePart type="family">Aasly</namePart><affiliation>Department of Neuroscience and Neurology, NTNU, Trondheim, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matthew J.</namePart><namePart type="family">Farrer</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Zbigniew K.</namePart><namePart type="family">Wszolek</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jon A.</namePart><namePart type="family">Stoessl</namePart><namePart type="termsOfAddress">MD, FRCPC</namePart><affiliation>Pacific Parkinson's Research Centre, Vancouver, British Columbia, Canada</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">2010-12-15</dateIssued><dateCaptured encoding="w3cdtf">2009-09-21</dateCaptured><dateValid encoding="w3cdtf">2010-05-10</dateValid><copyrightDate encoding="w3cdtf">2010</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">4</extent><extent unit="tables">2</extent><extent unit="references">38</extent><extent unit="words">5320</extent></physicalDescription><abstract lang="en">Increase in dopamine (DA) turnover was found to occur early in symptomatic Parkinson's disease (PD) and to be functionally related to the dopamine transporter (DAT). The objectives of this study were to examine changes in DA turnover in the asymptomatic PD phase; to compare them with changes in other dopaminergic markers, and to investigate a possible relationship between DAT and DA turnover. Eight subjects from families at increased risk of PD due to LRRK2 mutation were investigated. Positron emission tomography imaging was performed with: 18F‐fluorodopa to determine the effective DA distribution volume (EDV), the inverse of DA turnover, and the DA uptake rate Kocc, a marker of DA synthesis and storage; 11C‐methylphenidate (MP, a DAT marker) and 11C‐dihydrotetrabenazine (DTBZ, a VMAT2 marker) to estimate the binding potentials BPND_MP and BPND_DTBZ. On average, EDV showed the largest reduction from age‐matched control values (42%) followed by BPND _ MP (23%) and BPND _ DTBZ (17%), whereas Kocc remained in the normal range for all subjects. No correlation was found between EDV and any other marker. DA turnover was found to be elevated in asymptomatic mutation carriers at increased risk of PD. Such change was determined to be larger than and statistically independent from changes observed with the other markers. These results support a compensatory role of increased DA turnover in presymptomatic disease and indicate that at this stage, in contrast to the symptomatic PD phase, increased turnover is not related to DAT. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Authors do not report any conflict of interest or relevant financial interest in this manuscript.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>LRRK2 mutation</topic><topic>PET imaging</topic><topic>dopamine turnover</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></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>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>16</number></detail><extent unit="pages"><start>2717</start><end>2723</end><total>7</total></extent></part></relatedItem><identifier type="istex">2B49F1CFDF50DF88AA35CE307095DB569960BC13</identifier><identifier type="DOI">10.1002/mds.23356</identifier><identifier type="ArticleID">MDS23356</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 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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