Graft‐induced dyskinesias in Parkinson's disease: High striatal serotonin/dopamine transporter ratio
Identifieur interne : 002990 ( Istex/Corpus ); précédent : 002989; suivant : 002991Graft‐induced dyskinesias in Parkinson's disease: High striatal serotonin/dopamine transporter ratio
Auteurs : Marios Politis ; Wolfgang H. Oertel ; Kit Wu ; Niall P. Quinn ; Oliver Pogarell ; David J. Brooks ; Anders Bjorklund ; Olle Lindvall ; Paola PicciniSource :
- Movement Disorders [ 0885-3185 ] ; 2011-09.
English descriptors
Abstract
Graft‐induced dyskinesias are a serious complication after neural transplantation in Parkinson's disease. One patient with Parkinson's disease, treated with fetal grafts 14 years ago and deep brain stimulation 6 years ago, showed marked improvement of motor symptoms but continued to suffer from OFF‐medication graft‐induced dyskinesias. The patient received a series of clinical and imaging assessments. Positron emission tomography and single‐photon emission computed tomography 14 years posttransplantation revealed an elevated serotonin/dopamine transporter ratio in the grafted striatum compatible with serotonergic hyperinnervation. Inhibition of serotonin neuron activity by systemic administration of a 5‐HT1A agonist suppressed graft‐induced dyskinesias. Our data provide further evidence that serotonergic neurons mediate graft‐induced dyskinesias in Parkinson's disease. Achieving a normal striatal serotonin/dopamine transporter ratio following transplantation of fetal tissue or stem cells should be necessary to avoid the development of graft‐induced dyskinesias. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23743
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Achieving a normal striatal serotonin/dopamine transporter ratio following transplantation of fetal tissue or stem cells should be necessary to avoid the development of graft‐induced dyskinesias. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Marios Politis MD, PhD</name><affiliations><json:string>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom</json:string><json:string>Clinical Sciences Center, Medical Research Council, Hammersmith Hospital, Imperial College London, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Wolfgang H. 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One patient with Parkinson's disease, treated with fetal grafts 14 years ago and deep brain stimulation 6 years ago, showed marked improvement of motor symptoms but continued to suffer from OFF‐medication graft‐induced dyskinesias. The patient received a series of clinical and imaging assessments. Positron emission tomography and single‐photon emission computed tomography 14 years posttransplantation revealed an elevated serotonin/dopamine transporter ratio in the grafted striatum compatible with serotonergic hyperinnervation. Inhibition of serotonin neuron activity by systemic administration of a 5‐HT1A agonist suppressed graft‐induced dyskinesias. Our data provide further evidence that serotonergic neurons mediate graft‐induced dyskinesias in Parkinson's disease. 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type="correspondence"><p>Correspondence: Cyclotron Building, Hammersmith Hospital, Imperial College London, London W12 0NN, UK</p></note><affiliation>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><affiliation>Clinical Sciences Center, Medical Research Council, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation></author><author><persName><forename type="first">Wolfgang H.</forename><surname>Oertel</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurology, Philipps‐University, Marburg, Germany</affiliation></author><author><persName><forename type="first">Kit</forename><surname>Wu</surname><roleName type="degree">MRCP</roleName></persName><affiliation>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United 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creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Kit</givenNames><familyName>Wu</familyName><degrees>MRCP</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Niall P.</givenNames><familyName>Quinn</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Oliver</givenNames><familyName>Pogarell</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>David J.</givenNames><familyName>Brooks</familyName><degrees>MD, DSc, FRCP, FMedSci</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Anders</givenNames><familyName>Bjorklund</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af7 #af8"><personName><givenNames>Olle</givenNames><familyName>Lindvall</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Paola</givenNames><familyName>Piccini</familyName><degrees>MD, PhD, FRCP</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Clinical Sciences Center, Medical Research Council, Hammersmith Hospital, Imperial College London, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Philipps‐University, Marburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="GB" type="organization"><unparsedAffiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="DE" type="organization"><unparsedAffiliation>Department of Psychiatry, Ludwig‐Maximilian‐University of Munich, Munich, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="SE" type="organization"><unparsedAffiliation>Neurobiology Unit, Wallenberg Neuroscience Center, Lund, Sweden</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="SE" type="organization"><unparsedAffiliation>Laboratory of Neurogenesis and Cell Therapy, Wallenberg Neuroscience Center, Lund, Sweden</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="US" type="organization"><unparsedAffiliation>Lund Stem Cell Center, Lund, Sweden</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson</keyword><keyword xml:id="kwd2">transplantation</keyword><keyword xml:id="kwd3">dyskinesias</keyword><keyword xml:id="kwd4">serotonin transporter; dopamine transporter</keyword></keywordGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23743:MDS_23743_sm_suppinfomovie1"></mediaResource><caption>Supporting Information</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23743:MDS_23743_sm_suppinfomovie2"></mediaResource><caption>Supporting Information</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Graft‐induced dyskinesias are a serious complication after neural transplantation in Parkinson's disease. One patient with Parkinson's disease, treated with fetal grafts 14 years ago and deep brain stimulation 6 years ago, showed marked improvement of motor symptoms but continued to suffer from OFF‐medication graft‐induced dyskinesias. The patient received a series of clinical and imaging assessments. Positron emission tomography and single‐photon emission computed tomography 14 years posttransplantation revealed an elevated serotonin/dopamine transporter ratio in the grafted striatum compatible with serotonergic hyperinnervation. Inhibition of serotonin neuron activity by systemic administration of a 5‐HT<sub>1A</sub> agonist suppressed graft‐induced dyskinesias. Our data provide further evidence that serotonergic neurons mediate graft‐induced dyskinesias in Parkinson's disease. Achieving a normal striatal serotonin/dopamine transporter ratio following transplantation of fetal tissue or stem cells should be necessary to avoid the development of graft‐induced dyskinesias. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Relevant conflicts of interest/financial disclosures: Nothing to report.</p></note><note xml:id="fn2"><p>Full financial disclosures and author roles may be found in the online version of this article.</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>Graft‐induced dyskinesias in Parkinson's disease: High striatal serotonin/dopamine transporter ratio</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SERT/DAT in PD Patient with GIDS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Graft‐induced dyskinesias in Parkinson's disease: High striatal serotonin/dopamine transporter ratio</title></titleInfo><name type="personal"><namePart type="given">Marios</namePart><namePart type="family">Politis</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><affiliation>Clinical Sciences Center, Medical Research Council, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><description>Correspondence: Cyclotron Building, Hammersmith Hospital, Imperial College London, London W12 0NN, UK</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfgang H.</namePart><namePart type="family">Oertel</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Philipps‐University, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kit</namePart><namePart type="family">Wu</namePart><namePart type="termsOfAddress">MRCP</namePart><affiliation>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><affiliation>Clinical Sciences Center, Medical Research Council, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Niall P.</namePart><namePart type="family">Quinn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Oliver</namePart><namePart type="family">Pogarell</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Psychiatry, Ludwig‐Maximilian‐University of Munich, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Brooks</namePart><namePart type="termsOfAddress">MD, DSc, FRCP, FMedSci</namePart><affiliation>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><affiliation>Clinical Sciences Center, Medical Research Council, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anders</namePart><namePart type="family">Bjorklund</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurobiology Unit, Wallenberg Neuroscience Center, Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olle</namePart><namePart type="family">Lindvall</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Laboratory of Neurogenesis and Cell Therapy, Wallenberg Neuroscience Center, Lund, Sweden</affiliation><affiliation>Lund Stem Cell Center, Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Piccini</namePart><namePart type="termsOfAddress">MD, PhD, FRCP</namePart><affiliation>Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom</affiliation><affiliation>Clinical Sciences Center, Medical Research Council, Hammersmith Hospital, Imperial College London, London, United Kingdom</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">2011-09</dateIssued><dateCaptured encoding="w3cdtf">2011-01-22</dateCaptured><dateValid encoding="w3cdtf">2011-03-15</dateValid><copyrightDate encoding="w3cdtf">2011</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">1</extent><extent unit="references">20</extent><extent unit="words">4367</extent></physicalDescription><abstract lang="en">Graft‐induced dyskinesias are a serious complication after neural transplantation in Parkinson's disease. One patient with Parkinson's disease, treated with fetal grafts 14 years ago and deep brain stimulation 6 years ago, showed marked improvement of motor symptoms but continued to suffer from OFF‐medication graft‐induced dyskinesias. The patient received a series of clinical and imaging assessments. Positron emission tomography and single‐photon emission computed tomography 14 years posttransplantation revealed an elevated serotonin/dopamine transporter ratio in the grafted striatum compatible with serotonergic hyperinnervation. Inhibition of serotonin neuron activity by systemic administration of a 5‐HT1A agonist suppressed graft‐induced dyskinesias. Our data provide further evidence that serotonergic neurons mediate graft‐induced dyskinesias in Parkinson's disease. Achieving a normal striatal serotonin/dopamine transporter ratio following transplantation of fetal tissue or stem cells should be necessary to avoid the development of graft‐induced dyskinesias. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson</topic><topic>transplantation</topic><topic>dyskinesias</topic><topic>serotonin transporter; dopamine transporter</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information - Supporting Information - </note><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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1997</start><end>2003</end><total>7</total></extent></part></relatedItem><identifier type="istex">18EE56D4C431BCFCA2CE9F0A0F6D9A9CE2E412F4</identifier><identifier type="DOI">10.1002/mds.23743</identifier><identifier type="ArticleID">MDS23743</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 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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