Investigation into the pathogenesis of refractory neuropathies focusing on axon-myelin interaction.

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Axonal damage concomitant of inflammatory demyelination is one of the major factors for refractory or therapy-resistant peripheral neuropathies. In this study, we focused into transient axoglial glycoprotein-1 (TAG-1) which is related to axon-myelin interaction. We induced experimental autoimmune neuritis (EAN) on TAG-1 knockout (KO) mice and investigated phenotypes by clinicoelectrophysiological, and pathological analysis. As a result, the breakdown of the axon-myelin interaction could be associated to vulnerability of axonal function as well as refractory characteristics in inflammatory demyelinating neuropathies.