Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets
Identifieur interne : 000019 ( Istex/Corpus ); précédent : 000018; suivant : 000020Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets
Auteurs : Regina Katzenschlager ; Michael J. Jackson ; Sarah Rose ; Kim Stockwell ; Kayhan A. Tayarani-Binazir ; Mohammed Zubair ; Lance A. Smith ; Peter Jenner ; Andrew J. LeesSource :
- Movement Disorders [ 0885-3185 ] ; 2007-04-15.
English descriptors
Abstract
The neuropeptide melanocyte‐inhibiting factor (MIF) or L‐propyl‐L‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21256
Links to Exploration step
ISTEX:3A0D5F157B0A593D17D43EB7E889F5189630C0ADLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title><author><name sortKey="Katzenschlager, Regina" sort="Katzenschlager, Regina" uniqKey="Katzenschlager R" first="Regina" last="Katzenschlager">Regina Katzenschlager</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Donauspital/SMZ‐Ost, Vienna, Austria</mods:affiliation></affiliation></author><author><name sortKey="Jackson, Michael J" sort="Jackson, Michael J" uniqKey="Jackson M" first="Michael J." last="Jackson">Michael J. Jackson</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Rose, Sarah" sort="Rose, Sarah" uniqKey="Rose S" first="Sarah" last="Rose">Sarah Rose</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Stockwell, Kim" sort="Stockwell, Kim" uniqKey="Stockwell K" first="Kim" last="Stockwell">Kim Stockwell</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Tayarani Inazir, Kayhan A" sort="Tayarani Inazir, Kayhan A" uniqKey="Tayarani Inazir K" first="Kayhan A." last="Tayarani-Binazir">Kayhan A. Tayarani-Binazir</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Zubair, Mohammed" sort="Zubair, Mohammed" uniqKey="Zubair M" first="Mohammed" last="Zubair">Mohammed Zubair</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Smith, Lance A" sort="Smith, Lance A" uniqKey="Smith L" first="Lance A." last="Smith">Lance A. Smith</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew J. Lees</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Windeyer Building, 46 Cleveland Street, London W1 T 4JF, United Kingdom</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:3A0D5F157B0A593D17D43EB7E889F5189630C0AD</idno><date when="2007" year="2007">2007</date><idno type="doi">10.1002/mds.21256</idno><idno type="url">https://api.istex.fr/document/3A0D5F157B0A593D17D43EB7E889F5189630C0AD/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000019</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000019</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title><author><name sortKey="Katzenschlager, Regina" sort="Katzenschlager, Regina" uniqKey="Katzenschlager R" first="Regina" last="Katzenschlager">Regina Katzenschlager</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Donauspital/SMZ‐Ost, Vienna, Austria</mods:affiliation></affiliation></author><author><name sortKey="Jackson, Michael J" sort="Jackson, Michael J" uniqKey="Jackson M" first="Michael J." last="Jackson">Michael J. Jackson</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Rose, Sarah" sort="Rose, Sarah" uniqKey="Rose S" first="Sarah" last="Rose">Sarah Rose</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Stockwell, Kim" sort="Stockwell, Kim" uniqKey="Stockwell K" first="Kim" last="Stockwell">Kim Stockwell</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Tayarani Inazir, Kayhan A" sort="Tayarani Inazir, Kayhan A" uniqKey="Tayarani Inazir K" first="Kayhan A." last="Tayarani-Binazir">Kayhan A. Tayarani-Binazir</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Zubair, Mohammed" sort="Zubair, Mohammed" uniqKey="Zubair M" first="Mohammed" last="Zubair">Mohammed Zubair</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Smith, Lance A" sort="Smith, Lance A" uniqKey="Smith L" first="Lance A." last="Smith">Lance A. Smith</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew J. Lees</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Windeyer Building, 46 Cleveland Street, London W1 T 4JF, United Kingdom</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-04-15">2007-04-15</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="715">715</biblScope><biblScope unit="page" to="719">719</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3A0D5F157B0A593D17D43EB7E889F5189630C0AD</idno><idno type="DOI">10.1002/mds.21256</idno><idno type="ArticleID">MDS21256</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>dyskinesia</term><term>marmoset</term><term>melanocyte‐inhibiting factor (MIF)</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The neuropeptide melanocyte‐inhibiting factor (MIF) or L‐propyl‐L‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Regina Katzenschlager MD</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</json:string><json:string>Department of Neurology, Donauspital/SMZ‐Ost, Vienna, Austria</json:string></affiliations></json:item><json:item><name>Michael J. Jackson BSc</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</json:string></affiliations></json:item><json:item><name>Sarah Rose PhD</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</json:string></affiliations></json:item><json:item><name>Kim Stockwell PhD</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</json:string></affiliations></json:item><json:item><name>Kayhan A. Tayarani‐Binazir BSc</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</json:string></affiliations></json:item><json:item><name>Mohammed Zubair BSc</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</json:string></affiliations></json:item><json:item><name>Lance A. Smith PhD</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</json:string></affiliations></json:item><json:item><name>Peter Jenner DSc</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</json:string></affiliations></json:item><json:item><name>Andrew J. Lees MD, FRCP</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</json:string><json:string>Reta Lila Weston Institute of Neurological Studies, Windeyer Building, 46 Cleveland Street, London W1 T 4JF, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dyskinesia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>marmoset</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>melanocyte‐inhibiting factor (MIF)</value></json:item></subject><articleId><json:string>MDS21256</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The neuropeptide melanocyte‐inhibiting factor (MIF) or L‐propyl‐L‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society</abstract><qualityIndicators><score>4.926</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>946</abstractCharCount><pdfWordCount>3282</pdfWordCount><pdfCharCount>22235</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>137</abstractWordCount></qualityIndicators><title>Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title><genre><json:string>article</json:string></genre><host><volume>22</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>5</total><last>719</last><first>715</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Brief Report</value></json:item></subject><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1002/mds.21256</json:string></doi><id>3A0D5F157B0A593D17D43EB7E889F5189630C0AD</id><score>0.15820366</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/3A0D5F157B0A593D17D43EB7E889F5189630C0AD/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/3A0D5F157B0A593D17D43EB7E889F5189630C0AD/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3A0D5F157B0A593D17D43EB7E889F5189630C0AD/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Copyright © 2007 Movement Disorder Society</p></availability><date>2007</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title><author xml:id="author-1"><persName><forename type="first">Regina</forename><surname>Katzenschlager</surname></persName><roleName type="degree">MD</roleName><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</affiliation><affiliation>Department of Neurology, Donauspital/SMZ‐Ost, Vienna, Austria</affiliation></author><author xml:id="author-2"><persName><forename type="first">Michael J.</forename><surname>Jackson</surname></persName><roleName type="degree">BSc</roleName><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation></author><author xml:id="author-3"><persName><forename type="first">Sarah</forename><surname>Rose</surname></persName><roleName type="degree">PhD</roleName><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation></author><author xml:id="author-4"><persName><forename type="first">Kim</forename><surname>Stockwell</surname></persName><roleName type="degree">PhD</roleName><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation></author><author xml:id="author-5"><persName><forename type="first">Kayhan A.</forename><surname>Tayarani‐Binazir</surname></persName><roleName type="degree">BSc</roleName><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation></author><author xml:id="author-6"><persName><forename type="first">Mohammed</forename><surname>Zubair</surname></persName><roleName type="degree">BSc</roleName><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation></author><author xml:id="author-7"><persName><forename type="first">Lance A.</forename><surname>Smith</surname></persName><roleName type="degree">PhD</roleName><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation></author><author xml:id="author-8"><persName><forename type="first">Peter</forename><surname>Jenner</surname></persName><roleName type="degree">DSc</roleName><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation></author><author xml:id="author-9"><persName><forename type="first">Andrew J.</forename><surname>Lees</surname></persName><roleName type="degree">MD, FRCP</roleName><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</affiliation><affiliation>Reta Lila Weston Institute of Neurological Studies, Windeyer Building, 46 Cleveland Street, London W1 T 4JF, United Kingdom</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-04-15"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="715">715</biblScope><biblScope unit="page" to="719">719</biblScope></imprint></monogr><idno type="istex">3A0D5F157B0A593D17D43EB7E889F5189630C0AD</idno><idno type="DOI">10.1002/mds.21256</idno><idno type="ArticleID">MDS21256</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The neuropeptide melanocyte‐inhibiting factor (MIF) or L‐propyl‐L‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>Parkinson's disease</term></item><item><term>dyskinesia</term></item><item><term>marmoset</term></item><item><term>melanocyte‐inhibiting factor (MIF)</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-05-19">Received</change><change when="2006-08-19">Registration</change><change when="2007-04-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/3A0D5F157B0A593D17D43EB7E889F5189630C0AD/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. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley" registered="yes">10.1002/mds.v22:5</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2007-04-15">15 April 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="200" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.21256</doi><idGroup><id type="unit" value="MDS21256"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2007 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2006-05-19"></event><event type="manuscriptRevised" date="2006-08-01"></event><event type="manuscriptAccepted" date="2006-08-19"></event><event type="firstOnline" date="2007-03-20"></event><event type="publishedOnlineFinalForm" date="2007-04-25"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2007-03-20"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:FullText result:FullText" date="2011-02-24"></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">715</numbering><numbering type="pageLast">719</numbering></numberingGroup><correspondenceTo>Reta Lila Weston Institute of Neurological Studies, Windeyer Building, 46 Cleveland Street, London W1 T 4JF, United Kingdom</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21256.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="37"></count><count type="wordTotal" number="3274"></count></countGroup><titleGroup><title type="main" xml:lang="en">Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title><title type="short" xml:lang="en">Anti‐PD Activity of PLG or MIF in Marmosets</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Regina</givenNames><familyName>Katzenschlager</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Michael J.</givenNames><familyName>Jackson</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Sarah</givenNames><familyName>Rose</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Kim</givenNames><familyName>Stockwell</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Kayhan A.</givenNames><familyName>Tayarani‐Binazir</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Mohammed</givenNames><familyName>Zubair</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Lance A.</givenNames><familyName>Smith</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Peter</givenNames><familyName>Jenner</familyName><degrees>DSc</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Andrew J.</givenNames><familyName>Lees</familyName><degrees>MD, FRCP</degrees></personName><contactDetails><email normalForm="a-lees@ion.ucl.ac.uk">a‐lees@ion.ucl.ac.uk</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="AU" type="organization"><unparsedAffiliation>Department of Neurology, Donauspital/SMZ‐Ost, Vienna, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">dyskinesia</keyword><keyword xml:id="kwd3">marmoset</keyword><keyword xml:id="kwd4">melanocyte‐inhibiting factor (MIF)</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The neuropeptide melanocyte‐inhibiting factor (MIF) or <sc>L</sc>‐propyl‐<sc>L</sc>‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in <i>N</i>‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Anti‐PD Activity of PLG or MIF in Marmosets</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets</title></titleInfo><name type="personal"><namePart type="given">Regina</namePart><namePart type="family">Katzenschlager</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</affiliation><affiliation>Department of Neurology, Donauspital/SMZ‐Ost, Vienna, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael J.</namePart><namePart type="family">Jackson</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sarah</namePart><namePart type="family">Rose</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kim</namePart><namePart type="family">Stockwell</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kayhan A.</namePart><namePart type="family">Tayarani‐Binazir</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mohammed</namePart><namePart type="family">Zubair</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lance A.</namePart><namePart type="family">Smith</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurodegenerative Diseases Research Centre, King's College London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Jenner</namePart><namePart type="termsOfAddress">DSc</namePart><affiliation>Neurodegenerative Diseases Research Centre, King's College London, 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, FRCP</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom and National Hospital for Neurology and Neurosurgery, London, United Kingdom</affiliation><affiliation>Reta Lila Weston Institute of Neurological Studies, Windeyer Building, 46 Cleveland Street, London W1 T 4JF, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-04-15</dateIssued><dateCaptured encoding="w3cdtf">2006-05-19</dateCaptured><dateValid encoding="w3cdtf">2006-08-19</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">3</extent><extent unit="references">37</extent><extent unit="words">3274</extent></physicalDescription><abstract lang="en">The neuropeptide melanocyte‐inhibiting factor (MIF) or L‐propyl‐L‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society</abstract><subject lang="en"><genre>keywords</genre><topic>Parkinson's disease</topic><topic>dyskinesia</topic><topic>marmoset</topic><topic>melanocyte‐inhibiting factor (MIF)</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Brief Report</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>5</number></detail><extent unit="pages"><start>715</start><end>719</end><total>5</total></extent></part></relatedItem><identifier type="istex">3A0D5F157B0A593D17D43EB7E889F5189630C0AD</identifier><identifier type="DOI">10.1002/mds.21256</identifier><identifier type="ArticleID">MDS21256</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Psychologie/explor/DanceTherParkinsonV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000019 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000019 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Psychologie
|area= DanceTherParkinsonV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:3A0D5F157B0A593D17D43EB7E889F5189630C0AD
|texte= Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets
}}
| This area was generated with Dilib version V0.6.35. |  |