Multiple sclerosis (MS) is one of the most prominent demyelinating disorders with a phenotype of relapsing and remitting neurological deficits. The recurrence of relapse contributes to the accumulation of neuronal damage, which leads to the transition of the disease into secondaryprogressive MS (SPMS). The mechanisms of SPMS are unknown, making the invention of new therapeutic options for SPMS difficult. In the progressive phase, "glial inflammation" is assumed to be the major player in neurodegeneration. Recently, our group and others have shown that gap junction proteins called connexins are important in the pathomechanisms of SPMS in the context of "glial inflammation". The expression of glia in connexins differs between cell types. Astroglial connexins are down regulated in the acute phase and up regulated in the chronic phase of MS, while oligodendroglial connexins are down regulated through the course of the disease. The modification and malfunction of gap junction connexins are thought to play roles in the pathomechanisms of SPMS. Further elucidation of their mechanisms may provide clues useful for the invention of new therapeutic options for SPMS.
All Science Journal Classification (ASJC) codes
- Clinical Neurology