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Amantadine regulates the severity of experimental autoimmune encephalomyelitis
Author(s) -
Fukumoto Yuta,
Miyamoto Katsuichi,
Moriguchi Kota,
Kusunoki Susumu
Publication year - 2020
Publication title -
neurology and clinical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.125
0ISSN - 2049-4173
DOI - 10.1111/ncn3.12342
Subject(s) - amantadine , medicine , pharmacology , experimental autoimmune encephalomyelitis , foxp3 , encephalomyelitis , multiple sclerosis , immunology , fingolimod , immune system
Background Amantadine has been reported to have a neuroprotective effect, and it is therefore expected to have further clinical application. Aim In 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). Methods Experimental 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. Results Although 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. Conclusion Amantadine may be an effective therapy for inflammatory neurological diseases such as MS.