Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy
Identifieur interne : 001189 ( Istex/Corpus ); précédent : 001188; suivant : 001190Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy
Auteurs : Naomi M. Warren ; Margaret A. Piggott ; Elizabeth Greally ; Michelle Lake ; Andrew J. Lees ; David J. BurnSource :
- Movement Disorders [ 0885-3185 ] ; 2007-08-15.
English descriptors
Abstract
Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, 125I PE2I and dopamine D2 receptors, 125I epidepride) and cholinergic (nicotinic α4β2 receptors, 125I 5IA85380 and muscarinic M1 receptors, 3H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic M1 receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21573
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ISTEX:1BC8FD9B9FF157AB7022B2DC10AE2D59F99113ECLe document en format XML
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In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, 125I PE2I and dopamine D2 receptors, 125I epidepride) and cholinergic (nicotinic α4β2 receptors, 125I 5IA85380 and muscarinic M1 receptors, 3H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic M1 receptors were unchanged compared with controls. 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Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, 125I PE2I and dopamine D2 receptors, 125I epidepride) and cholinergic (nicotinic α4β2 receptors, 125I 5IA85380 and muscarinic M1 receptors, 3H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic M1 receptors were unchanged compared with controls. 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Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="110"><doi origin="wiley" registered="yes">10.1002/mds.v22:11</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue">11</numbering></numberingGroup><coverDate startDate="2007-08-15">15 August 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.21573</doi><idGroup><id type="unit" value="MDS21573"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2007 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2006-11-21"></event><event type="manuscriptRevised" date="2007-02-28"></event><event type="manuscriptAccepted" date="2007-04-13"></event><event type="publishedOnlineEarlyUnpaginated" date="2007-05-29"></event><event type="firstOnline" date="2007-05-29"></event><event type="publishedOnlineFinalForm" date="2007-08-29"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" 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">1594</numbering><numbering type="pageLast">1600</numbering></numberingGroup><correspondenceTo>Wolfson Research centre, Institute for Ageing and Health, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, United Kingdom</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21573.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="59"></count><count type="wordTotal" number="5116"></count></countGroup><titleGroup><title type="main" xml:lang="en">Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy</title><title type="short" xml:lang="en">Dopaminergic and Cholinergic Function in PSP</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Naomi M.</givenNames><familyName>Warren</familyName><degrees>MD</degrees></personName><contactDetails><email>naomiwarren@doctors.org.uk</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Margaret A.</givenNames><familyName>Piggott</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Elizabeth</givenNames><familyName>Greally</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michelle</givenNames><familyName>Lake</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Andrew J.</givenNames><familyName>Lees</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>David J.</givenNames><familyName>Burn</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Sara Koe PSP Research Centre, Institute of Neurology, University College, London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">dopaminergic</keyword><keyword xml:id="kwd2">cholinergic</keyword><keyword xml:id="kwd3">progressive supranuclear palsy</keyword><keyword xml:id="kwd4">basal ganglia</keyword></keywordGroup><fundingInfo><fundingAgency>PSP (Europe) Association</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Eloise Troxel Memorial Research Grant</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, <sup>125</sup>I PE2I and dopamine D2 receptors, <sup>125</sup>I epidepride) and cholinergic (nicotinic α4β2 receptors, <sup>125</sup>I 5IA85380 and muscarinic M1 receptors, <sup>3</sup>H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic M1 receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors. © 2007 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>Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dopaminergic and Cholinergic Function in PSP</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy</title></titleInfo><name type="personal"><namePart type="given">Naomi M.</namePart><namePart type="family">Warren</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom</affiliation><description>Correspondence: Wolfson Research centre, Institute for Ageing and Health, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, United Kingdom</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Margaret A.</namePart><namePart type="family">Piggott</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elizabeth</namePart><namePart type="family">Greally</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michelle</namePart><namePart type="family">Lake</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew J.</namePart><namePart type="family">Lees</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom</affiliation><affiliation>Sara Koe PSP Research Centre, Institute of Neurology, University College, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Burn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne, 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">2007-08-15</dateIssued><dateCaptured encoding="w3cdtf">2006-11-21</dateCaptured><dateValid encoding="w3cdtf">2007-04-13</dateValid><copyrightDate encoding="w3cdtf">2007</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">1</extent><extent unit="tables">3</extent><extent unit="references">59</extent><extent unit="words">5116</extent></physicalDescription><abstract lang="en">Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, 125I PE2I and dopamine D2 receptors, 125I epidepride) and cholinergic (nicotinic α4β2 receptors, 125I 5IA85380 and muscarinic M1 receptors, 3H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic M1 receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors. © 2007 Movement Disorder Society</abstract><note type="funding">PSP (Europe) Association</note><note type="funding">Eloise Troxel Memorial Research Grant</note><subject lang="en"><genre>Keywords</genre><topic>dopaminergic</topic><topic>cholinergic</topic><topic>progressive supranuclear palsy</topic><topic>basal ganglia</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>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>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1594</start><end>1600</end><total>7</total></extent></part></relatedItem><identifier type="istex">1BC8FD9B9FF157AB7022B2DC10AE2D59F99113EC</identifier><identifier type="DOI">10.1002/mds.21573</identifier><identifier type="ArticleID">MDS21573</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 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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