Do dopamine agonists or levodopa modify Parkinson's disease progression?
Identifieur interne : 000321 ( Main/Corpus ); précédent : 000320; suivant : 000322Do dopamine agonists or levodopa modify Parkinson's disease progression?
Auteurs : K. Marek ; D. Jennings ; J. SeibylSource :
- European Journal of Neurology [ 1351-5101 ] ; 2002-11.
English descriptors
- KwdEn :
Abstract
During the past decade, in vivo imaging of the nigrostriatal dopaminergic system has been developed as a research tool to monitor progressive dopaminergic neuron loss in Parkinson's disease (PD) and to assess the effect of medication on imaging outcomes. Recently two similar studies compared the effect of initial treatment with a dopamine agonist (pramipexole (CALM‐PD CIT) or ropinirole (REAL‐PET)) or levodopa on the progression of PD as measured by [123I]β‐CIT or [18F]Dopa imaging. These two clinical imaging studies targeting dopamine function with different imaging ligands and technology both demonstrate slowing in the rate of loss of [123I]β‐CIT or [18F]Dopa uptake in early PD patients treated with dopamine agonists compared with levodopa. The relative reduction in the per cent loss from baseline of [123I]β‐CIT uptake in the pramipexole versus the levodopa group was 47% at 22 months, 44% at 34 months and 37% at 46 months after initiating treatment. The relative reduction of 18F‐dopa uptake in the ropinirole group versus the levodopa group was 35% at 24 months. These results should be very cautiously interpreted with regard to the effect of dopamine agonists or levodopa on clinical disease progression. These data highlight the need to compare imaging outcomes of dopamine neuronal loss with multiple meaningful clinical endpoints of disease progression in placebo controlled, larger and long‐term studies.
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DOI: 10.1046/j.1468-1331.9.s3.2.x
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Recently two similar studies compared the effect of initial treatment with a dopamine agonist (pramipexole (CALM‐PD CIT) or ropinirole (REAL‐PET)) or levodopa on the progression of PD as measured by [123I]β‐CIT or [18F]Dopa imaging. These two clinical imaging studies targeting dopamine function with different imaging ligands and technology both demonstrate slowing in the rate of loss of [123I]β‐CIT or [18F]Dopa uptake in early PD patients treated with dopamine agonists compared with levodopa. The relative reduction in the per cent loss from baseline of [123I]β‐CIT uptake in the pramipexole versus the levodopa group was 47% at 22 months, 44% at 34 months and 37% at 46 months after initiating treatment. The relative reduction of 18F‐dopa uptake in the ropinirole group versus the levodopa group was 35% at 24 months. These results should be very cautiously interpreted with regard to the effect of dopamine agonists or levodopa on clinical disease progression. 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Marek, Institute for Neurodegenerative Disorders, 60 Temple St/Suite 8B, New Haven, CT 06510, USA (tel.: + 1 203 401 4300; fax: + 1 203 401 4301; e‐mail: <email>kmarek@indd.org</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE0076.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="1"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="50"></count><count type="wordTotal" number="5549272"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Do dopamine agonists or levodopa modify Parkinson's disease progression?</title><title type="shortAuthors">K. Marek <i>et al.</i></title><title type="short">Dopamine agonists, levodopa and Parkinson's disease progression</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>K.</givenNames><familyName>Marek</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>D.</givenNames><familyName>Jennings</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>J.</givenNames><familyName>Seibyl</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation><i>The Institute for Neurodegenerative Disorders, New Haven, CT, USA</i></unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">dopamine transporter</keyword><keyword xml:id="k2">neuroprotection</keyword><keyword xml:id="k3">PET</keyword><keyword xml:id="k4">SPECT</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>During the past decade, <i>in vivo</i> imaging of the nigrostriatal dopaminergic system has been developed as a research tool to monitor progressive dopaminergic neuron loss in Parkinson's disease (PD) and to assess the effect of medication on imaging outcomes. Recently two similar studies compared the effect of initial treatment with a dopamine agonist (pramipexole (CALM‐PD CIT) or ropinirole (REAL‐PET)) or levodopa on the progression of PD as measured by [<sup>123</sup>I]<i>β</i>‐CIT or [<sup>18</sup>F]Dopa imaging. These two clinical imaging studies targeting dopamine function with different imaging ligands and technology both demonstrate slowing in the rate of loss of [<sup>123</sup>I]<i>β</i>‐CIT or [<sup>18</sup>F]Dopa uptake in early PD patients treated with dopamine agonists compared with levodopa. The relative reduction in the per cent loss from baseline of [<sup>123</sup>I]<i>β</i>‐CIT uptake in the pramipexole versus the levodopa group was 47% at 22 months, 44% at 34 months and 37% at 46 months after initiating treatment. The relative reduction of <sup>18</sup>F‐dopa uptake in the ropinirole group versus the levodopa group was 35% at 24 months. These results should be very cautiously interpreted with regard to the effect of dopamine agonists or levodopa on clinical disease progression. These data highlight the need to compare imaging outcomes of dopamine neuronal loss with multiple meaningful clinical endpoints of disease progression in placebo controlled, larger and long‐term studies.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Do dopamine agonists or levodopa modify Parkinson's disease progression?</title></titleInfo><titleInfo type="abbreviated"><title>Dopamine agonists, levodopa and Parkinson's disease progression</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Do dopamine agonists or levodopa modify Parkinson's disease progression?</title></titleInfo><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Marek</namePart><affiliation>The Institute for Neurodegenerative Disorders, New Haven, CT, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Jennings</namePart><affiliation>The Institute for Neurodegenerative Disorders, New Haven, CT, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Seibyl</namePart><affiliation>The Institute for Neurodegenerative Disorders, New Haven, CT, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science, Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2002-11</dateIssued><copyrightDate encoding="w3cdtf">2002</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">1</extent><extent unit="references">50</extent><extent unit="words">5549272</extent></physicalDescription><abstract lang="en">During the past decade, in vivo imaging of the nigrostriatal dopaminergic system has been developed as a research tool to monitor progressive dopaminergic neuron loss in Parkinson's disease (PD) and to assess the effect of medication on imaging outcomes. Recently two similar studies compared the effect of initial treatment with a dopamine agonist (pramipexole (CALM‐PD CIT) or ropinirole (REAL‐PET)) or levodopa on the progression of PD as measured by [123I]β‐CIT or [18F]Dopa imaging. These two clinical imaging studies targeting dopamine function with different imaging ligands and technology both demonstrate slowing in the rate of loss of [123I]β‐CIT or [18F]Dopa uptake in early PD patients treated with dopamine agonists compared with levodopa. The relative reduction in the per cent loss from baseline of [123I]β‐CIT uptake in the pramipexole versus the levodopa group was 47% at 22 months, 44% at 34 months and 37% at 46 months after initiating treatment. The relative reduction of 18F‐dopa uptake in the ropinirole group versus the levodopa group was 35% at 24 months. These results should be very cautiously interpreted with regard to the effect of dopamine agonists or levodopa on clinical disease progression. These data highlight the need to compare imaging outcomes of dopamine neuronal loss with multiple meaningful clinical endpoints of disease progression in placebo controlled, larger and long‐term studies.</abstract><subject lang="en"><genre>Keywords</genre><topic>dopamine transporter</topic><topic>neuroprotection</topic><topic>PET</topic><topic>SPECT</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s3</number></detail><extent unit="pages"><start>15</start><end>22</end><total>8</total></extent></part></relatedItem><identifier type="istex">98A9381E777339AA3416C686EDC110F5A0499845</identifier><identifier type="DOI">10.1046/j.1468-1331.9.s3.2.x</identifier><identifier type="ArticleID">ENE0076</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science, Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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