Nigrostriatal upregulation of 5‐HT2A receptors correlates with motor dysfunction in progressive supranuclear palsy
Identifieur interne : 002E10 ( Istex/Corpus ); précédent : 002E09; suivant : 002E11Nigrostriatal upregulation of 5‐HT2A receptors correlates with motor dysfunction in progressive supranuclear palsy
Auteurs : Maria Stamelou ; Andreas Matusch ; David Elmenhorst ; René Hurlemann ; Karla M. Eggert ; Karl Zilles ; Wolfgang H. Oertel ; Günter U. Höglinger ; Andreas BauerSource :
- Movement Disorders [ 0885-3185 ] ; 2009-06-15.
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Abstract
A dysfunction of multiple neurotransmitter systems is assumed as a neurochemical basis of the akinetic‐rigid syndrome of progressive supranuclear palsy (PSP). In vitro studies have produced conflicting results on the serotoninergic system in PSP. We, therefore, studied the binding potential of the serotonin 2A (5‐HT2A) receptor ligand [18F]altanserin in 8 patients with clinically probable PSP and 13 healthy controls using positron emission tomography. We found an up‐regulation of 5‐HT2A receptors in the substantia nigra and, to a lower degree, in the striatum, while neocortical 5‐ HT2A receptor densities showed no changes upon partial‐volume correction. Nigral and striatal receptor changes were significantly correlated with patients' scores of motor dysfunction (UPDRS III, PSP‐rating scale) pointing to a functional relevance of the described findings. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22533
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Oertel</name><affiliation><mods:affiliation>Department of Neurology, Philipps University, Marburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hoglinger, Gunter U" sort="Hoglinger, Gunter U" uniqKey="Hoglinger G" first="Günter U." last="Höglinger">Günter U. Höglinger</name><affiliation><mods:affiliation>Department of Neurology, Philipps University, Marburg, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bauer, Andreas" sort="Bauer, Andreas" uniqKey="Bauer A" first="Andreas" last="Bauer">Andreas Bauer</name><affiliation><mods:affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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In vitro studies have produced conflicting results on the serotoninergic system in PSP. We, therefore, studied the binding potential of the serotonin 2A (5‐HT2A) receptor ligand [18F]altanserin in 8 patients with clinically probable PSP and 13 healthy controls using positron emission tomography. We found an up‐regulation of 5‐HT2A receptors in the substantia nigra and, to a lower degree, in the striatum, while neocortical 5‐ HT2A receptor densities showed no changes upon partial‐volume correction. Nigral and striatal receptor changes were significantly correlated with patients' scores of motor dysfunction (UPDRS III, PSP‐rating scale) pointing to a functional relevance of the described findings. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Maria Stamelou MD</name><affiliations><json:string>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</json:string><json:string>Department of Neurology, Philipps University, Marburg, Germany</json:string></affiliations></json:item><json:item><name>Andreas Matusch MD</name><affiliations><json:string>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</json:string><json:string>Department of Neurology, Philipps University, Marburg, Germany</json:string></affiliations></json:item><json:item><name>David Elmenhorst MD</name><affiliations><json:string>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</json:string></affiliations></json:item><json:item><name>René Hurlemann MD, PhD</name><affiliations><json:string>Department of Psychiatry, University of Bonn, Bonn, Germany</json:string></affiliations></json:item><json:item><name>Karla M. Eggert MD</name><affiliations><json:string>Department of Neurology, Philipps University, Marburg, Germany</json:string></affiliations></json:item><json:item><name>Karl Zilles MD</name><affiliations><json:string>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</json:string><json:string>C. & O. Vogt Institute for Brain Research, University of Düsseldorf, Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Wolfgang H. Oertel MD</name><affiliations><json:string>Department of Neurology, Philipps University, Marburg, Germany</json:string></affiliations></json:item><json:item><name>Günter U. Höglinger MD</name><affiliations><json:string>Department of Neurology, Philipps University, Marburg, Germany</json:string><json:string>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</json:string></affiliations></json:item><json:item><name>Andreas Bauer MD</name><affiliations><json:string>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</json:string><json:string>Department of Neurology, University of Düsseldorf, Düsseldorf, Germany</json:string><json:string>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>PSP</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Steele‐Richardson‐Olszewski syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>serotonin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>5‐HT</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>5‐HT2A receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item></subject><language><json:string>eng</json:string></language><abstract>A dysfunction of multiple neurotransmitter systems is assumed as a neurochemical basis of the akinetic‐rigid syndrome of progressive supranuclear palsy (PSP). In vitro studies have produced conflicting results on the serotoninergic system in PSP. We, therefore, studied the binding potential of the serotonin 2A (5‐HT2A) receptor ligand [18F]altanserin in 8 patients with clinically probable PSP and 13 healthy controls using positron emission tomography. We found an up‐regulation of 5‐HT2A receptors in the substantia nigra and, to a lower degree, in the striatum, while neocortical 5‐ HT2A receptor densities showed no changes upon partial‐volume correction. Nigral and striatal receptor changes were significantly correlated with patients' scores of motor dysfunction (UPDRS III, PSP‐rating scale) pointing to a functional relevance of the described findings. © 2009 Movement Disorder Society</abstract><qualityIndicators><score>4.234</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>896</abstractCharCount><pdfWordCount>2722</pdfWordCount><pdfCharCount>17963</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>126</abstractWordCount></qualityIndicators><title>Nigrostriatal upregulation of 5‐HT2A receptors correlates with motor dysfunction in progressive supranuclear palsy</title><genre><json:string>Serial article</json:string></genre><host><volume>24</volume><pages><total>6</total><last>1175</last><first>1170</first></pages><issn><json:string>0885-3185</json:string></issn><issue>8</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1002/mds.22533</json:string></doi><id>C9C7F6F48A73FC841BA75DE92A7EA650E09C4457</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/C9C7F6F48A73FC841BA75DE92A7EA650E09C4457/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/C9C7F6F48A73FC841BA75DE92A7EA650E09C4457/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/C9C7F6F48A73FC841BA75DE92A7EA650E09C4457/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Nigrostriatal upregulation of 5‐HT2A receptors correlates with motor dysfunction in progressive supranuclear palsy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2009</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None reported.</note><note>Brain Imaging Center West (BICW)</note><note>German Federal Ministry for Education and Research - No. BMBF, grant 01 GI9934;</note><note>Deutsche Forschungsgemeinschaft - No. DFG, Klinische Forschergruppe 112; No. HO2402/6‐1;</note><note>International Consortium for Brain Mapping</note><note>Willy Robert Pitzer Foundation</note><note>von behring|röntgen|stiftung - No. 56‐0039;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Nigrostriatal upregulation of 5‐HT2A receptors correlates with motor dysfunction in progressive supranuclear palsy</title><author><persName><forename type="first">Maria</forename><surname>Stamelou</surname><roleName type="degree">MD</roleName></persName><note type="biography">The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</note><affiliation>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</affiliation><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation></author><author><persName><forename type="first">Andreas</forename><surname>Matusch</surname><roleName type="degree">MD</roleName></persName><note type="biography">The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</note><affiliation>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</affiliation><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation></author><author><persName><forename type="first">David</forename><surname>Elmenhorst</surname><roleName type="degree">MD</roleName></persName><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation></author><author><persName><forename type="first">René</forename><surname>Hurlemann</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Psychiatry, University of Bonn, Bonn, Germany</affiliation></author><author><persName><forename type="first">Karla M.</forename><surname>Eggert</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation></author><author><persName><forename type="first">Karl</forename><surname>Zilles</surname><roleName type="degree">MD</roleName></persName><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>C. & O. Vogt Institute for Brain Research, University of Düsseldorf, Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Wolfgang H.</forename><surname>Oertel</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation></author><author><persName><forename type="first">Günter U.</forename><surname>Höglinger</surname><roleName type="degree">MD</roleName></persName><note type="biography">The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</note><affiliation>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</affiliation><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation><affiliation>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</affiliation></author><author><persName><forename type="first">Andreas</forename><surname>Bauer</surname><roleName type="degree">MD</roleName></persName><note type="biography">The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</note><affiliation>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</affiliation><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>Department of Neurology, University of Düsseldorf, Düsseldorf, Germany</affiliation><affiliation>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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In vitro studies have produced conflicting results on the serotoninergic system in PSP. We, therefore, studied the binding potential of the serotonin 2A (5‐HT2A) receptor ligand [18F]altanserin in 8 patients with clinically probable PSP and 13 healthy controls using positron emission tomography. We found an up‐regulation of 5‐HT2A receptors in the substantia nigra and, to a lower degree, in the striatum, while neocortical 5‐ HT2A receptor densities showed no changes upon partial‐volume correction. Nigral and striatal receptor changes were significantly correlated with patients' scores of motor dysfunction (UPDRS III, PSP‐rating scale) pointing to a functional relevance of the described findings. © 2009 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>PSP</term></item><item><term>Steele‐Richardson‐Olszewski syndrome</term></item><item><term>serotonin</term></item><item><term>5‐HT</term></item><item><term>5‐HT2A receptor</term></item><item><term>PET</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="2008-10-17">Received</change><change when="2009-02-16">Registration</change><change when="2009-06-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/C9C7F6F48A73FC841BA75DE92A7EA650E09C4457/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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Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, Germany</line><line>Andreas Bauer, Institute of Neuroscience and Biophysics–Medicine (<i>INB‐3)</i>, Research Center Jülich, Jülich 52425, Germany</line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS22533.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="18"></count><count type="wordTotal" number="3192"></count></countGroup><titleGroup><title type="main" xml:lang="en">Nigrostriatal upregulation of 5‐HT<sub>2A</sub> receptors correlates with motor dysfunction in progressive supranuclear palsy<link href="#fn1"></link></title><title type="short" xml:lang="en">[<sup>18</sup>F]Altanserin PET in PSP</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" noteRef="#fn2"><personName><givenNames>Maria</givenNames><familyName>Stamelou</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2" noteRef="#fn2"><personName><givenNames>Andreas</givenNames><familyName>Matusch</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>David</givenNames><familyName>Elmenhorst</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>René</givenNames><familyName>Hurlemann</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Karla M.</givenNames><familyName>Eggert</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af4"><personName><givenNames>Karl</givenNames><familyName>Zilles</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Wolfgang H.</givenNames><familyName>Oertel</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2" corresponding="yes" noteRef="#fn2"><personName><givenNames>Günter U.</givenNames><familyName>Höglinger</familyName><degrees>MD</degrees></personName><contactDetails><email normalForm="guenter.hoeglinger@med.uni-marburg.de">guenter.hoeglinger@med.uni‐marburg.de</email></contactDetails></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af5" corresponding="yes" noteRef="#fn2"><personName><givenNames>Andreas</givenNames><familyName>Bauer</familyName><degrees>MD</degrees></personName><contactDetails><email normalForm="an.bauer@fz-juelich.de">an.bauer@fz‐juelich.de</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Philipps University, Marburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Psychiatry, University of Bonn, Bonn, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>C. & O. Vogt Institute for Brain Research, University of Düsseldorf, Düsseldorf, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University of Düsseldorf, Düsseldorf, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">PSP</keyword><keyword xml:id="kwd2">Steele‐Richardson‐Olszewski syndrome</keyword><keyword xml:id="kwd3">serotonin</keyword><keyword xml:id="kwd4">5‐HT</keyword><keyword xml:id="kwd5">5‐HT<sub>2A</sub> receptor</keyword><keyword xml:id="kwd6">PET</keyword></keywordGroup><fundingInfo><fundingAgency>Brain Imaging Center West (BICW)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>German Federal Ministry for Education and Research</fundingAgency><fundingNumber>BMBF, grant 01 GI9934</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Deutsche Forschungsgemeinschaft</fundingAgency><fundingNumber>DFG, Klinische Forschergruppe 112</fundingNumber><fundingNumber>HO2402/6‐1</fundingNumber></fundingInfo><fundingInfo><fundingAgency>International Consortium for Brain Mapping</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Willy Robert Pitzer Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>von behring|röntgen|stiftung</fundingAgency><fundingNumber>56‐0039</fundingNumber></fundingInfo><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:mds22533:MDS_22533_sm_supptable1"></mediaResource><caption>Supporting Table 1. Partial volume‐corrected 5‐HT2A binding potential (BPP) in anatomically defined volumes of interest (VOI).</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>A dysfunction of multiple neurotransmitter systems is assumed as a neurochemical basis of the akinetic‐rigid syndrome of progressive supranuclear palsy (PSP). In vitro studies have produced conflicting results on the serotoninergic system in PSP. We, therefore, studied the binding potential of the serotonin 2A (5‐HT<sub>2A</sub>) receptor ligand [<link href="#bib18">18</link>F]altanserin in 8 patients with clinically probable PSP and 13 healthy controls using positron emission tomography. We found an up‐regulation of 5‐HT<sub>2A</sub> receptors in the substantia nigra and, to a lower degree, in the striatum, while neocortical 5‐ HT<sub>2A</sub> receptor densities showed no changes upon partial‐volume correction. Nigral and striatal receptor changes were significantly correlated with patients' scores of motor dysfunction (UPDRS III, PSP‐rating scale) pointing to a functional relevance of the described findings. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</p></note><note xml:id="fn2"><p>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Nigrostriatal upregulation of 5‐HT2A receptors correlates with motor dysfunction in progressive supranuclear palsy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>[18F]Altanserin PET in PSP</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Nigrostriatal upregulation of 5‐HT</title></titleInfo><name type="personal"><namePart type="given">Maria</namePart><namePart type="family">Stamelou</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation><description>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andreas</namePart><namePart type="family">Matusch</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation><description>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Elmenhorst</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">René</namePart><namePart type="family">Hurlemann</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Psychiatry, University of Bonn, Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karla M.</namePart><namePart type="family">Eggert</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karl</namePart><namePart type="family">Zilles</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>C. & O. Vogt Institute for Brain Research, University of Düsseldorf, Düsseldorf, Germany</affiliation><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</namePart><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Günter U.</namePart><namePart type="family">Höglinger</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Philipps University, Marburg, Germany</affiliation><description>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</description><affiliation>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andreas</namePart><namePart type="family">Bauer</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neuroscience and Biophysics–Medicine (INB‐3), Research Center Jülich, Jülich, Germany</affiliation><affiliation>Department of Neurology, University of Düsseldorf, Düsseldorf, Germany</affiliation><description>The first two authors contributed equally to this study, and the last two author's contributed equally to this study.</description><affiliation>Günter U. Höglinger, Department of Neurology, Philipps University, Rudolf‐Bultmann Str. 8, Marburg 35039, GermanyAndreas Bauer, Institute of Neuroscience and Biophysics–Medicine (, Research Center Jülich, Jülich 52425, Germany</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">2009-06-15</dateIssued><dateCaptured encoding="w3cdtf">2008-10-17</dateCaptured><dateValid encoding="w3cdtf">2009-02-16</dateValid><copyrightDate encoding="w3cdtf">2009</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">1</extent><extent unit="references">18</extent><extent unit="words">3192</extent></physicalDescription><abstract lang="en">A dysfunction of multiple neurotransmitter systems is assumed as a neurochemical basis of the akinetic‐rigid syndrome of progressive supranuclear palsy (PSP). In vitro studies have produced conflicting results on the serotoninergic system in PSP. We, therefore, studied the binding potential of the serotonin 2A (5‐HT2A) receptor ligand [18F]altanserin in 8 patients with clinically probable PSP and 13 healthy controls using positron emission tomography. We found an up‐regulation of 5‐HT2A receptors in the substantia nigra and, to a lower degree, in the striatum, while neocortical 5‐ HT2A receptor densities showed no changes upon partial‐volume correction. Nigral and striatal receptor changes were significantly correlated with patients' scores of motor dysfunction (UPDRS III, PSP‐rating scale) pointing to a functional relevance of the described findings. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">Brain Imaging Center West (BICW)</note><note type="funding">German Federal Ministry for Education and Research - No. BMBF, grant 01 GI9934; </note><note type="funding">Deutsche Forschungsgemeinschaft - No. DFG, Klinische Forschergruppe 112; No. HO2402/6‐1; </note><note type="funding">International Consortium for Brain Mapping</note><note type="funding">Willy Robert Pitzer Foundation</note><note type="funding">von behring|röntgen|stiftung - No. 56‐0039; </note><subject lang="en"><genre>Keywords</genre><topic>PSP</topic><topic>Steele‐Richardson‐Olszewski syndrome</topic><topic>serotonin</topic><topic>5‐HT</topic><topic>5‐HT2A receptor</topic><topic>PET</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 Table 1. Partial volume‐corrected 5‐HT2A binding potential (BPP) in anatomically defined volumes of interest (VOI). - </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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1170</start><end>1175</end><total>6</total></extent></part></relatedItem><identifier type="istex">C9C7F6F48A73FC841BA75DE92A7EA650E09C4457</identifier><identifier type="DOI">10.1002/mds.22533</identifier><identifier type="ArticleID">MDS22533</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 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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