Neuroprotective effect of riluzole in a primate model of Parkinson's disease: Behavioral and histological evidence
Identifieur interne : 004374 ( Main/Curation ); précédent : 004373; suivant : 004375Neuroprotective 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.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Adult animal, Animals, Behavior, Animal (drug effects), Benzothiazole, Callithrix, Chemotherapy, Disease Models, Animal, Dopamine (metabolism), Dopamine Agents (adverse effects), Dopaminergic neuron, Female, Immunohistochemistry, Locomotion (drug effects), MPTP, Male, Monkey, Motricity, Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Neuroprotective agent, Nissl Bodies (drug effects), Nissl Bodies (metabolism), Nissl Bodies (pathology), Parkinson Disease (drug therapy), Parkinson Disease, Secondary (chemically induced), Parkinson disease, Pathology, Prognosis, Psychotropic, Random Allocation, Riluzole, Riluzole (pharmacology), Riluzole (therapeutic use), Substantia Nigra (drug effects), Treatment, locomotor impairment, neurological deficit, neuronal loss, neuroprotection, riluzole.
- MESH :
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Behavior, Animal, Locomotion, Nissl Bodies, Substantia Nigra.
- drug therapy : Parkinson Disease.
- chemical , metabolism : Dopamine, Nissl Bodies.
- pathology : Nissl Bodies.
- chemical , pharmacology : Neuroprotective Agents, Riluzole.
- chemical , therapeutic use : Neuroprotective Agents, Riluzole.
- Animals, Callithrix, Disease Models, Animal, Female, Immunohistochemistry, Male, Random Allocation.
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.
Url:
DOI: 10.1002/mds.1272
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<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>
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<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.</div>
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<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>
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