Neuroprotective effect of riluzole in a primate model of Parkinson's disease: Behavioral and histological evidence
Identifieur interne : 006379 ( Main/Merge ); précédent : 006378; suivant : 006380Neuroprotective effect of riluzole in a primate model of Parkinson's disease: Behavioral and histological evidence
Auteurs : Maria C. Obinu [France] ; Michel Reibaud [France] ; Véronique Blanchard [France] ; Saliha Moussaoui [France] ; Assunta Imperato [France]Source :
- 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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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-01">2002-01</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="13">13</biblScope><biblScope unit="page" to="19">19</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E192C410F7C9A7500EF9CF5991DFCD8D876A3FF6</idno><idno type="DOI">10.1002/mds.1272</idno><idno type="ArticleID">MDS1272</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>MPTP</term><term>locomotor impairment</term><term>neurological deficit</term><term>neuronal loss</term><term>neuroprotection</term><term>riluzole</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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