Neuroprotective effect of riluzole in a primate model of Parkinson's disease: Behavioral and histological evidence
Identifieur interne : 001026 ( Istex/Corpus ); précédent : 001025; suivant : 001027Neuroprotective effect of riluzole in a primate model of Parkinson's disease: Behavioral and histological evidence
Auteurs : Maria C. Obinu ; Michel Reibaud ; Véronique Blanchard ; Saliha Moussaoui ; Assunta ImperatoSource :
- Movement Disorders [ 0885-3185 ] ; 2002-01.
English descriptors
Abstract
Our study aimed to determine whether riluzole, which has shown efficacy as a disease‐modifying agent in amyotrophic lateral sclerosis (ALS), is neuroprotective in a marmoset model of Parkinson's disease (PD). Reduction of energy demand by riluzole could be a rational neuroprotective strategy with good tolerability. The efficacy of riluzole was evaluated in marmosets by testing its ability to reduce MPTP‐induced behavioral deficits and loss of dopaminergic nigral neurons. Marmosets were divided into two groups of four animals each: animals in Group 1 were injected twice with MPTP (2 mg/kg subcutaneous) and treated with riluzole (10 mg/kg per os b.i.d.), animals in Group 2 (controls) were injected with MPTP and with the vehicle of riluzole. A third group of marmosets which did not receive MPTP or riluzole drug was introduced for neurohistopathological studies (normal animals). Marmosets treated with riluzole preserved a better motor function and neurological performance through the 26 days of assessment when compared with the controls. Histologically, there was sparing of TH‐ and Nissl‐stained nigral neurons and of TH‐stained terminals in the striatum and the putamen in the group treated with riluzole compared to the controls. We conclude that riluzole protects dopaminergic neurons and reduces behavioral deficits in a marmoset model of PD. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1272
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ISTEX:E192C410F7C9A7500EF9CF5991DFCD8D876A3FF6Le document en format XML
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Reduction of energy demand by riluzole could be a rational neuroprotective strategy with good tolerability. The efficacy of riluzole was evaluated in marmosets by testing its ability to reduce MPTP‐induced behavioral deficits and loss of dopaminergic nigral neurons. Marmosets were divided into two groups of four animals each: animals in Group 1 were injected twice with MPTP (2 mg/kg subcutaneous) and treated with riluzole (10 mg/kg per os b.i.d.), animals in Group 2 (controls) were injected with MPTP and with the vehicle of riluzole. A third group of marmosets which did not receive MPTP or riluzole drug was introduced for neurohistopathological studies (normal animals). Marmosets treated with riluzole preserved a better motor function and neurological performance through the 26 days of assessment when compared with the controls. 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Histologically, there was sparing of TH‐ and Nissl‐stained nigral neurons and of TH‐stained terminals in the striatum and the putamen in the group treated with riluzole compared to the controls. We conclude that riluzole protects dopaminergic neurons and reduces behavioral deficits in a marmoset model of PD. © 2001 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>MPTP</term></item><item><term>locomotor impairment</term></item><item><term>neurological deficit</term></item><item><term>neuronal loss</term></item><item><term>neuroprotection</term></item><item><term>riluzole</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="2001-03-08">Received</change><change when="2001-06-25">Registration</change><change when="2002-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E192C410F7C9A7500EF9CF5991DFCD8D876A3FF6/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>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</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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Vitry sur Seine, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">MPTP</keyword><keyword xml:id="kwd2">locomotor impairment</keyword><keyword xml:id="kwd3">neurological deficit</keyword><keyword xml:id="kwd4">neuronal loss</keyword><keyword xml:id="kwd5">neuroprotection</keyword><keyword xml:id="kwd6">riluzole</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Our study aimed to determine whether riluzole, which has shown efficacy as a disease‐modifying agent in amyotrophic lateral sclerosis (ALS), is neuroprotective in a marmoset model of Parkinson's disease (PD). Reduction of energy demand by riluzole could be a rational neuroprotective strategy with good tolerability. The efficacy of riluzole was evaluated in marmosets by testing its ability to reduce MPTP‐induced behavioral deficits and loss of dopaminergic nigral neurons. Marmosets were divided into two groups of four animals each: animals in Group 1 were injected twice with MPTP (2 mg/kg subcutaneous) and treated with riluzole (10 mg/kg per os b.i.d.), animals in Group 2 (controls) were injected with MPTP and with the vehicle of riluzole. A third group of marmosets which did not receive MPTP or riluzole drug was introduced for neurohistopathological studies (normal animals). Marmosets treated with riluzole preserved a better motor function and neurological performance through the 26 days of assessment when compared with the controls. Histologically, there was sparing of TH‐ and Nissl‐stained nigral neurons and of TH‐stained terminals in the striatum and the putamen in the group treated with riluzole compared to the controls. 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Vitry sur Seine, France</affiliation><description>Correspondence: Neurodegenerative Diseases Program, Research Center of Paris, Aventis Pharma, 13 quai Jules Guesde BP‐14, Vitry sur Seine, France, 94403</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michel</namePart><namePart type="family">Reibaud</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurodegenerative Disease Program, Research Center of Paris, Aventis Pharma, S.A. Vitry sur Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Véronique</namePart><namePart type="family">Blanchard</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurodegenerative Disease Program, Research Center of Paris, Aventis Pharma, S.A. Vitry sur Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Saliha</namePart><namePart type="family">Moussaoui</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurodegenerative Disease Program, Research Center of Paris, Aventis Pharma, S.A. Vitry sur Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Assunta</namePart><namePart type="family">Imperato</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurodegenerative Disease Program, Research Center of Paris, Aventis Pharma, S.A. Vitry sur Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-01</dateIssued><dateCaptured encoding="w3cdtf">2001-03-08</dateCaptured><dateValid encoding="w3cdtf">2001-06-25</dateValid><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="references">41</extent><extent unit="words">4037</extent></physicalDescription><abstract lang="en">Our study aimed to determine whether riluzole, which has shown efficacy as a disease‐modifying agent in amyotrophic lateral sclerosis (ALS), is neuroprotective in a marmoset model of Parkinson's disease (PD). Reduction of energy demand by riluzole could be a rational neuroprotective strategy with good tolerability. The efficacy of riluzole was evaluated in marmosets by testing its ability to reduce MPTP‐induced behavioral deficits and loss of dopaminergic nigral neurons. Marmosets were divided into two groups of four animals each: animals in Group 1 were injected twice with MPTP (2 mg/kg subcutaneous) and treated with riluzole (10 mg/kg per os b.i.d.), animals in Group 2 (controls) were injected with MPTP and with the vehicle of riluzole. A third group of marmosets which did not receive MPTP or riluzole drug was introduced for neurohistopathological studies (normal animals). Marmosets treated with riluzole preserved a better motor function and neurological performance through the 26 days of assessment when compared with the controls. Histologically, there was sparing of TH‐ and Nissl‐stained nigral neurons and of TH‐stained terminals in the striatum and the putamen in the group treated with riluzole compared to the controls. We conclude that riluzole protects dopaminergic neurons and reduces behavioral deficits in a marmoset model of PD. © 2001 Movement Disorder Society.</abstract><subject lang="en"><genre>Keywords</genre><topic>MPTP</topic><topic>locomotor impairment</topic><topic>neurological deficit</topic><topic>neuronal loss</topic><topic>neuroprotection</topic><topic>riluzole</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>13</start><end>19</end><total>7</total></extent></part></relatedItem><identifier type="istex">E192C410F7C9A7500EF9CF5991DFCD8D876A3FF6</identifier><identifier type="DOI">10.1002/mds.1272</identifier><identifier type="ArticleID">MDS1272</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>John Wiley & Sons, Inc.</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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