Dopaminergic and cholinergic lesions in progressive supranuclear palsy
Identifieur interne : 001665 ( Main/Corpus ); précédent : 001664; suivant : 001666Dopaminergic and cholinergic lesions in progressive supranuclear palsy
Auteurs : Merle Ruberg ; France Javoy-Agid ; Etienne Hirsch ; Bernard Scatton ; Rémy Lheureux ; Jean-Jacques Hauw ; Charles Duyckaerts ; Françloise Gray ; Ariel Morel-Maroger ; André Rascol ; Michel Serdaru ; AgidSource :
- Annals of Neurology [ 0364-5134 ] ; 1985-11.
Abstract
In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.
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DOI: 10.1002/ana.410180503
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V. Couturier, 92220 Bagneux, France</mods:affiliation></affiliation></author><author><name sortKey="Lheureux, Remy" sort="Lheureux, Remy" uniqKey="Lheureux R" first="Rémy" last="Lheureux">Rémy Lheureux</name><affiliation><mods:affiliation>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</mods:affiliation></affiliation></author><author><name sortKey="Hauw, Jean Acques" sort="Hauw, Jean Acques" uniqKey="Hauw J" first="Jean-Jacques" last="Hauw">Jean-Jacques Hauw</name><affiliation><mods:affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Duyckaerts, Charles" sort="Duyckaerts, Charles" uniqKey="Duyckaerts C" first="Charles" last="Duyckaerts">Charles Duyckaerts</name><affiliation><mods:affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Gray, Francloise" sort="Gray, Francloise" uniqKey="Gray F" first="Françloise" last="Gray">Françloise Gray</name><affiliation><mods:affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Morel Aroger, Ariel" sort="Morel Aroger, Ariel" uniqKey="Morel Aroger A" first="Ariel" last="Morel-Maroger">Ariel Morel-Maroger</name><affiliation><mods:affiliation>Hôpital de Corbeil‐Essones, 91 Corbeil Essonnes, France</mods:affiliation></affiliation></author><author><name sortKey="Rascol, Andre" sort="Rascol, Andre" uniqKey="Rascol A" first="André" last="Rascol">André Rascol</name><affiliation><mods:affiliation>Hôpital Purpan, 31 Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Serdaru, Michel" sort="Serdaru, Michel" uniqKey="Serdaru M" first="Michel" last="Serdaru">Michel Serdaru</name><affiliation><mods:affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Agid" sort="Agid" uniqKey="Agid" last="Agid">Agid</name><affiliation><mods:affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Little, Brown and Company</publisher><pubPlace>Boston</pubPlace><date type="published" when="1985-11">1985-11</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="523">523</biblScope><biblScope unit="page" to="529">529</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">ED5C79FF895C5038FEE8C38B0834F33C52B85A1A</idno><idno type="DOI">10.1002/ana.410180503</idno><idno type="ArticleID">ANA410180503</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Merle Ruberg PhD</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item><json:item><name>France Javoy‐Agid PhD</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item><json:item><name>Etienne Hirsch MS</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item><json:item><name>Bernard Scatton PhD</name><affiliations><json:string>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</json:string></affiliations></json:item><json:item><name>Rémy Lheureux</name><affiliations><json:string>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</json:string></affiliations></json:item><json:item><name>Jean‐Jacques Hauw MD</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item><json:item><name>Charles Duyckaerts MD</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item><json:item><name>Françloise Gray MD</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item><json:item><name>Ariel Morel‐Maroger MD</name><affiliations><json:string>Hôpital de Corbeil‐Essones, 91 Corbeil Essonnes, France</json:string></affiliations></json:item><json:item><name>André Rascol MD</name><affiliations><json:string>Hôpital Purpan, 31 Toulouse, France</json:string></affiliations></json:item><json:item><name>Michel Serdaru MD</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item><json:item><name>Dr. Agid MD</name><affiliations><json:string>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</json:string></affiliations></json:item></author><articleId><json:string>ANA410180503</json:string></articleId><language><json:string>eng</json:string></language><abstract>In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.</abstract><qualityIndicators><score>6.853</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 828 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1520</abstractCharCount><pdfWordCount>4297</pdfWordCount><pdfCharCount>27566</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>213</abstractWordCount></qualityIndicators><title>Dopaminergic and cholinergic lesions in progressive supranuclear palsy</title><genre><json:string>article</json:string></genre><host><volume>18</volume><publisherId><json:string>ANA</json:string></publisherId><pages><total>7</total><last>529</last><first>523</first></pages><issn><json:string>0364-5134</json:string></issn><issue>5</issue><subject><json:item><value>Original Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8249</json:string></eissn><title>Annals of Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><publicationDate>1985</publicationDate><copyrightDate>1985</copyrightDate><doi><json:string>10.1002/ana.410180503</json:string></doi><id>ED5C79FF895C5038FEE8C38B0834F33C52B85A1A</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/ED5C79FF895C5038FEE8C38B0834F33C52B85A1A/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/ED5C79FF895C5038FEE8C38B0834F33C52B85A1A/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/ED5C79FF895C5038FEE8C38B0834F33C52B85A1A/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Dopaminergic and cholinergic lesions in progressive supranuclear palsy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Little, Brown and Company</publisher><pubPlace>Boston</pubPlace><availability><p>WILEY</p></availability><date>1985</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Dopaminergic and cholinergic lesions in progressive supranuclear palsy</title><author><persName><forename type="first">Merle</forename><surname>Ruberg</surname></persName><roleName type="degree">PhD</roleName><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author><author><persName><forename type="first">France</forename><surname>Javoy‐Agid</surname></persName><roleName type="degree">PhD</roleName><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author><author><persName><forename type="first">Etienne</forename><surname>Hirsch</surname></persName><roleName type="degree">MS</roleName><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author><author><persName><forename type="first">Bernard</forename><surname>Scatton</surname></persName><roleName type="degree">PhD</roleName><affiliation>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</affiliation></author><author><persName><forename type="first">Rémy</forename><surname>Lheureux</surname></persName><affiliation>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</affiliation></author><author><persName><forename type="first">Jean‐Jacques</forename><surname>Hauw</surname></persName><roleName type="degree">MD</roleName><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author><author><persName><forename type="first">Charles</forename><surname>Duyckaerts</surname></persName><roleName type="degree">MD</roleName><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author><author><persName><forename type="first">Françloise</forename><surname>Gray</surname></persName><roleName type="degree">MD</roleName><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author><author><persName><forename type="first">Ariel</forename><surname>Morel‐Maroger</surname></persName><roleName type="degree">MD</roleName><affiliation>Hôpital de Corbeil‐Essones, 91 Corbeil Essonnes, France</affiliation></author><author><persName><forename type="first">André</forename><surname>Rascol</surname></persName><roleName type="degree">MD</roleName><affiliation>Hôpital Purpan, 31 Toulouse, France</affiliation></author><author><persName><forename type="first">Michel</forename><surname>Serdaru</surname></persName><roleName type="degree">MD</roleName><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author><author><persName><surname>Agid</surname></persName><roleName type="degree">Dr.</roleName><note type="correspondence"><p>Correspondence: Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</p></note><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Little, Brown and Company</publisher><pubPlace>Boston</pubPlace><date type="published" when="1985-11"></date><biblScope unit="volume">18</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="523">523</biblScope><biblScope unit="page" to="529">529</biblScope></imprint></monogr><idno type="istex">ED5C79FF895C5038FEE8C38B0834F33C52B85A1A</idno><idno type="DOI">10.1002/ana.410180503</idno><idno type="ArticleID">ANA410180503</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1985</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1984-11-26">Received</change><change when="1985-02-28">Registration</change><change when="1985-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/ED5C79FF895C5038FEE8C38B0834F33C52B85A1A/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>Little, Brown 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number="7"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1985 American Neurological Association</copyright><eventGroup><event type="manuscriptReceived" date="1984-11-26"></event><event type="manuscriptRevised" date="1985-02-28"></event><event type="manuscriptAccepted" date="1985-02-28"></event><event type="firstOnline" date="2004-10-07"></event><event type="publishedOnlineFinalForm" date="2004-10-07"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.15 mode:FullText source:HeaderRef result:HeaderRef" date="2010-07-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">523</numbering><numbering type="pageLast">529</numbering></numberingGroup><correspondenceTo>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA410180503.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="6"></count><count type="referenceTotal" number="34"></count></countGroup><titleGroup><title type="main" xml:lang="en">Dopaminergic and cholinergic lesions in progressive supranuclear palsy</title><title type="short" xml:lang="en">PSP: Dopaminergic and Cholinergic Lesions</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Merle</givenNames><familyName>Ruberg</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>France</givenNames><familyName>Javoy‐Agid</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Etienne</givenNames><familyName>Hirsch</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Bernard</givenNames><familyName>Scatton</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Rémy</givenNames><familyName>Lheureux</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jean‐Jacques</givenNames><familyName>Hauw</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Charles</givenNames><familyName>Duyckaerts</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Françloise</givenNames><familyName>Gray</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Ariel</givenNames><familyName>Morel‐Maroger</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af4"><personName><givenNames>André</givenNames><familyName>Rascol</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michel</givenNames><familyName>Serdaru</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Yves</givenNames><familyName>Agid</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Hôpital de Corbeil‐Essones, 91 Corbeil Essonnes, France</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>Hôpital Purpan, 31 Toulouse, France</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [<sup>3</sup>H]spiperone and [<sup>3</sup>H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [<sup>3</sup>H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dopaminergic and cholinergic lesions in progressive supranuclear palsy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PSP: Dopaminergic and Cholinergic Lesions</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Dopaminergic and cholinergic lesions in progressive supranuclear palsy</title></titleInfo><name type="personal"><namePart type="given">Merle</namePart><namePart type="family">Ruberg</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">France</namePart><namePart type="family">Javoy‐Agid</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Etienne</namePart><namePart type="family">Hirsch</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bernard</namePart><namePart type="family">Scatton</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rémy</namePart><namePart type="family">Lheureux</namePart><affiliation>Synthélabo—LERS, Boulevard P. V. Couturier, 92220 Bagneux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Jacques</namePart><namePart type="family">Hauw</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Charles</namePart><namePart type="family">Duyckaerts</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Françloise</namePart><namePart type="family">Gray</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ariel</namePart><namePart type="family">Morel‐Maroger</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Hôpital de Corbeil‐Essones, 91 Corbeil Essonnes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">André</namePart><namePart type="family">Rascol</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Hôpital Purpan, 31 Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michel</namePart><namePart type="family">Serdaru</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Agid</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</affiliation><description>Correspondence: Laboratoire de Medécine Expérimentale, Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 91 Boulevard de l'Hǒpital, 75005 Paris, France</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Little, Brown and Company</publisher><place><placeTerm type="text">Boston</placeTerm></place><dateIssued encoding="w3cdtf">1985-11</dateIssued><dateCaptured encoding="w3cdtf">1984-11-26</dateCaptured><dateValid encoding="w3cdtf">1985-02-28</dateValid><copyrightDate encoding="w3cdtf">1985</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="tables">6</extent><extent unit="references">34</extent></physicalDescription><abstract lang="en">In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>523</start><end>529</end><total>7</total></extent></part></relatedItem><identifier type="istex">ED5C79FF895C5038FEE8C38B0834F33C52B85A1A</identifier><identifier type="DOI">10.1002/ana.410180503</identifier><identifier type="ArticleID">ANA410180503</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1985 American Neurological Association</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Little, Brown and Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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