Lipoic acid decreases inflammation and confers neuroprotection in experimental autoimmune optic neuritis.

Lipoic acid (LA) is an antioxidant that is effective in treating experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS). C57BL/6 mice with EAE develop experimental autoimmune optic neuritis (EAON), which models acute optic neuritis in humans. Here we determined whether LA is therapeutically effective in EAON. We immunized C57BL/6 mice with MOG 35-55 peptide. Mice received either daily subcutaneous injections of LA (100mg/kg) or saline in early or late suppression paradigms. In the early suppression paradigm, optic nerve cross-sections showed 14.9±3.8% (mean±SEM) damage in mice receiving saline (n=7) and 2.0±0.4% damage in mice given LA (n=7, p=0.001). In the late suppression paradigm, optic nerve sections showed 24.6±3.5% damage in mice treated with saline (n=7) and 8.4±2.5% in mice treated with LA (n=7, p=0.004). Thus a dramatic reduction in axonal injury was seen after LA administration in both experimental paradigms. Compared with saline treated mice with EAON, optic nerves from mice receiving LA had significantly fewer CD4+ and CD11b+ cells in both paradigms. This study provides a rationale for investigating the therapeutic efficacy of LA in acute optic neuritis in humans.