Amantadine regulates the severity of experimental autoimmune encephalomyelitis

Abstract

AbstractBackgroundAmantadine has been reported to have a neuroprotective effect, and it is therefore expected to have further clinical application.AimIn this study, we examined the therapeutic effect of the N‐methyl‐D‐aspartate (NMDA) receptor antagonist amantadine on experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS).MethodsExperimental autoimmune encephalomyelitis was induced in C57BL/6 mice. Amantadine was administered at doses of 40 mg/kg dissolved in phosphate buffer saline (PBS) by feeding cannula every other day. The control group received PBS only. The immunized mice were examined and scored daily until day 35. T‐cell proliferation assay, pathological analysis, and analysis of regulatory cells were performed.ResultsAlthough amantadine did not significantly suppress the incidence or severity of EAE, it significantly reduced clinical symptoms in the recovery phase. There was also a significant increase in CD4+ CD25+ Foxp3+ T cells in response to amantadine treatment. These results suggest that amantadine promotes symptom recovery in EAE by acting in an immunosuppressive manner.ConclusionAmantadine may be an effective therapy for inflammatory neurological diseases such as MS.