Long‐term changes of striatal dopamine D2 Receptors in patients with Parkinson's disease: A study with positron emission tomography and [11C]Raclopride
Identifieur interne : 001697 ( Istex/Corpus ); précédent : 001696; suivant : 001698Long‐term changes of striatal dopamine D2 Receptors in patients with Parkinson's disease: A study with positron emission tomography and [11C]Raclopride
Auteurs : Angelo Antonini ; Johannes Schwarz ; Wolfgang H. Oertel ; Oliver Pogarell ; LeendersSource :
- Movement Disorders [ 0885-3185 ] ; 1997-01.
English descriptors
Abstract
We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug‐naive stage and 3–5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3–5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at “off” had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3–4 months after therapy began and at that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long‐term downregulation of striatal dopamine D2 receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.
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DOI: 10.1002/mds.870120107
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Long‐term changes of striatal dopamine D2 Receptors in patients with Parkinson's disease: A study with positron emission tomography and [11C]Raclopride</title><author><name sortKey="Antonini, Angelo" sort="Antonini, Angelo" uniqKey="Antonini A" first="Angelo" last="Antonini">Angelo Antonini</name><affiliation><mods:affiliation>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Schwarz, Johannes" sort="Schwarz, Johannes" uniqKey="Schwarz J" first="Johannes" last="Schwarz">Johannes Schwarz</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Oertel, Wolfgang H" sort="Oertel, Wolfgang H" uniqKey="Oertel W" first="Wolfgang H." last="Oertel">Wolfgang H. Oertel</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Pogarell, Oliver" sort="Pogarell, Oliver" uniqKey="Pogarell O" first="Oliver" last="Pogarell">Oliver Pogarell</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Leenders" sort="Leenders" uniqKey="Leenders" last="Leenders">Leenders</name><affiliation><mods:affiliation>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:B6E9D4BE9B82257D2DDDF0C976C381F6BA037634</idno><date when="1997" year="1997">1997</date><idno type="doi">10.1002/mds.870120107</idno><idno type="url">https://api.istex.fr/document/B6E9D4BE9B82257D2DDDF0C976C381F6BA037634/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001697</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Long‐term changes of striatal dopamine D2 Receptors in patients with Parkinson's disease: A study with positron emission tomography and [11C]Raclopride</title><author><name sortKey="Antonini, Angelo" sort="Antonini, Angelo" uniqKey="Antonini A" first="Angelo" last="Antonini">Angelo Antonini</name><affiliation><mods:affiliation>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Schwarz, Johannes" sort="Schwarz, Johannes" uniqKey="Schwarz J" first="Johannes" last="Schwarz">Johannes Schwarz</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Oertel, Wolfgang H" sort="Oertel, Wolfgang H" uniqKey="Oertel W" first="Wolfgang H." last="Oertel">Wolfgang H. Oertel</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Pogarell, Oliver" sort="Pogarell, Oliver" uniqKey="Pogarell O" first="Oliver" last="Pogarell">Oliver Pogarell</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Leenders" sort="Leenders" uniqKey="Leenders" last="Leenders">Leenders</name><affiliation><mods:affiliation>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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="1997-01">1997-01</date><biblScope unit="vol">12</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="33">33</biblScope><biblScope unit="page" to="38">38</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">B6E9D4BE9B82257D2DDDF0C976C381F6BA037634</idno><idno type="DOI">10.1002/mds.870120107</idno><idno type="ArticleID">MDS870120107</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine D2 receptors</term><term>Parkinson's disease</term><term>Positron emission tomography</term><term>[11C]Raclopride</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug‐naive stage and 3–5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3–5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at “off” had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3–4 months after therapy began and at that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long‐term downregulation of striatal dopamine D2 receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Angelo Antonini</name><affiliations><json:string>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</json:string></affiliations></json:item><json:item><name>Johannes Schwarz</name><affiliations><json:string>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</json:string></affiliations></json:item><json:item><name>Wolfgang H. Oertel</name><affiliations><json:string>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</json:string></affiliations></json:item><json:item><name>Oliver Pogarell</name><affiliations><json:string>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</json:string></affiliations></json:item><json:item><name>Prof. Leenders</name><affiliations><json:string>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</json:string><json:string>Department of Neurology, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Positron emission tomography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>[11C]Raclopride</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine D2 receptors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug‐naive stage and 3–5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p > 0.04). The caudate nucleus revealed values in the normal range. After 3–5 years, RACLO binding was significantly reduced in the putamen (p > 0.03) and caudate nucleus (p > 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p > 0.05). The clinical score at “off” had significantly worsened (p > 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3–4 months after therapy began and at that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long‐term downregulation of striatal dopamine D2 receptor binding in PD. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1997-01"></date><biblScope unit="vol">12</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="33">33</biblScope><biblScope unit="page" to="38">38</biblScope></imprint></monogr><idno type="istex">B6E9D4BE9B82257D2DDDF0C976C381F6BA037634</idno><idno type="DOI">10.1002/mds.870120107</idno><idno type="ArticleID">MDS870120107</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug‐naive stage and 3–5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3–5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at “off” had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3–4 months after therapy began and at that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long‐term downregulation of striatal dopamine D2 receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Positron emission tomography</term></item><item><term>[11C]Raclopride</term></item><item><term>Dopamine D2 receptors</term></item><item><term>Parkinson's disease</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-10-23">Received</change><change when="1996-03-27">Registration</change><change when="1997-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/B6E9D4BE9B82257D2DDDF0C976C381F6BA037634/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. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/mds.v12:1</doi><numberingGroup><numbering type="journalVolume" number="12">12</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="1997-01">January 1997</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="7" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870120107</doi><idGroup><id type="unit" value="MDS870120107"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1997 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1995-10-23"></event><event type="manuscriptRevised" date="1996-03-26"></event><event type="manuscriptAccepted" date="1996-03-27"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" 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">33</numbering><numbering type="pageLast">38</numbering></numberingGroup><correspondenceTo>PET Department, Paul Scherrer Institute, CH‐5232 Villigen, Switzerland</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870120107.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="23"></count></countGroup><titleGroup><title type="main" xml:lang="en">Long‐term changes of striatal dopamine D<sub>2</sub> Receptors in patients with Parkinson's disease: A study with positron emission tomography and [<sup>11</sup>C]Raclopride</title><title type="short" xml:lang="en">LONG‐TERM DOPAMINE D<sub>2</sub> RECEPTOR CHANGES IN PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Angelo</givenNames><familyName>Antonini</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Johannes</givenNames><familyName>Schwarz</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Wolfgang H.</givenNames><familyName>Oertel</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Oliver</givenNames><familyName>Pogarell</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af3" corresponding="yes"><personName><honorifics>Prof.</honorifics><givenNames>Klaus L.</givenNames><familyName>Leenders</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CH" type="organization"><unparsedAffiliation>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CH" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Positron emission tomography</keyword><keyword xml:id="kwd2">[<sup>11</sup>C]Raclopride</keyword><keyword xml:id="kwd3">Dopamine D<sub>2</sub> receptors</keyword><keyword xml:id="kwd4">Parkinson's disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We used [<sup>11</sup>C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D<sub>2</sub> receptor binding in nine patients with Parkinson's disease (PD) at an early drug‐naive stage and 3–5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3–5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at “off” had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3–4 months after therapy began and at that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long‐term downregulation of striatal dopamine D<sub>2</sub> receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Long‐term changes of striatal dopamine D2 Receptors in patients with Parkinson's disease: A study with positron emission tomography and [11C]Raclopride</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>LONG‐TERM DOPAMINE D2 RECEPTOR CHANGES IN PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Long‐term changes of striatal dopamine D</title></titleInfo><name type="personal"><namePart type="given">Angelo</namePart><namePart type="family">Antonini</namePart><affiliation>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Johannes</namePart><namePart type="family">Schwarz</namePart><affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfgang H.</namePart><namePart type="family">Oertel</namePart><affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Oliver</namePart><namePart type="family">Pogarell</namePart><affiliation>Department of Neurology, University Hospital Zurich, Zurich, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Prof.</namePart><namePart type="family">Leenders</namePart><affiliation>PET Department, Paul Scherrer Institute, Villigen, University Hospital Zurich, Zurich, Switzerland</affiliation><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</affiliation><description>Correspondence: PET Department, Paul Scherrer Institute, CH‐5232 Villigen, Switzerland</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">1997-01</dateIssued><dateCaptured encoding="w3cdtf">1995-10-23</dateCaptured><dateValid encoding="w3cdtf">1996-03-27</dateValid><copyrightDate encoding="w3cdtf">1997</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">2</extent><extent unit="references">23</extent></physicalDescription><abstract lang="en">We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug‐naive stage and 3–5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3–5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at “off” had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3–4 months after therapy began and at that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long‐term downregulation of striatal dopamine D2 receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.</abstract><subject lang="en"><genre>Keywords</genre><topic>Positron emission tomography</topic><topic>[11C]Raclopride</topic><topic>Dopamine D2 receptors</topic><topic>Parkinson's disease</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>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>1997</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>33</start><end>38</end><total>6</total></extent></part></relatedItem><identifier type="istex">B6E9D4BE9B82257D2DDDF0C976C381F6BA037634</identifier><identifier type="DOI">10.1002/mds.870120107</identifier><identifier type="ArticleID">MDS870120107</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 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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