Objective: The present study was initiated to evaluate a possible relationship between CD14 monocyte receptor genetic polymorphism and the risk of Parkinson's disease (PD). Background: Inflammatory processes have been postulated to play a role in the pathogenesis of PD. The C(Ϫ260) 3 T polymorphism
Poster session 4, Abstracts 1131–1166
- Book ID
- 102503211
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 234 KB
- Volume
- 19
- Category
- Article
- ISSN
- 0885-3185
No coin nor oath required. For personal study only.
✦ Synopsis
Only symptomatic treatments of limited efficacy are available in striatonigral degeneration (SND)/multiple system atrophy-parkinsonism (MSA-P). We investigated the potency of riluzole, an anti-glutamatergic drug, to jam the neuronal death process in a phenotypic MPTP ϩ 3-nitropropionic acid mouse model of SND/MSA-P. We used a "neuronal rescue" strategy by administering riluzole (for 7 days) only after the end of intoxication. The motor disorder, its recovery, behavioral performances at motor and sensorimotor integration tests (rotarod, pole test, traversing a beam, open-field), and histopathological outcome were compared in the control (saline, n ϭ 7) and riluzole groups (10 mg/kg, n ϭ 7; 20 mg/kg, n ϭ 7), matched by triplets for motor severity. While riluzole did not produce any effect on the gross motor disorder nor on rotarod task or open-field kinetic variables, riluzole allowed better recovery on the beamtraversing task and the pole test. Accordingly, the histopathological outcome was significantly better in the riluzole-treated mice regarding both nigral and dorsolateral striatal cell loss and astroglial activation, with a dose-effect relationship. Thus, riluzole induces subtle symptomatic effects but has "neuronal rescue" properties in a SND/MSA-P phenotypic animal model.
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