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Prophylactic exposure to oral riluzole reduces the clinical severity and immune-related biomarkers of experimental autoimmune encephalomyelitis

Glutamate-mediated excitotoxicity and immune cell infiltration are hallmarks of multiple sclerosis. The glutamate release inhibitor, riluzole (RIL), has been shown to attenuate the clinical symptoms of experimental autoimmune encephalomyelitis (EAE) in mice, but an association between glutamate exci...

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Bibliographic Details
Published in:Journal of neuroimmunology 2021-07, Vol.356, p.577603-577603, Article 577603
Main Authors: Rotolo, Renee A., Demuro, Jennifer, Drummond, Gregory, Little, Casey, Johns, Lennart D., Betz, Adrienne J.
Format: Article
Language:English
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Summary:Glutamate-mediated excitotoxicity and immune cell infiltration are hallmarks of multiple sclerosis. The glutamate release inhibitor, riluzole (RIL), has been shown to attenuate the clinical symptoms of experimental autoimmune encephalomyelitis (EAE) in mice, but an association between glutamate excitotoxicity and the progression of MOG35-55-induced EAE has not been well defined. This study investigated the effects of prophylactic and chronic oral RIL on the clinical severity of EAE. Prophylactic+chronic RIL reduced the presence of inflammatory infiltrates, altered GFAP and Foxp3, and attenuated disease severity. These findings indicate a need to delineate the distinct role of glutamate in EAE symptomatology. [Display omitted] •Riluzole (RIL) attenuates the clinical symptoms of experimental autoimmune encephalomyelitis (EAE) in mice.•The treatment regimen of oral RIL (prophylacticversus chronic) affects clinical severity of EAE.•Glutamate signaling plays a role in EAE symptomatology.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2021.577603