Association between axonal damage and molecular basis in demyelinating neuropathies: prognosis and response to treatment

轴突-髓鞘相互作用与从Ranvie结到Anastaparanode的几种功能分子之间的关联是公认的。本研究采用酶联免疫吸附法（ELISA）检测脱髓鞘性神经病患者神经组织中钠通道、TAG-1、CNTN 1、Caspr和Caspr 2等分子的分布和表达。光镜下无形态学改变，但脱髓鞘神经病组钠通道表达明显减少。此外，我们证实同源TAG-1敲除小鼠导致显著的发育不全。这些结果可能表明，与轴突-髓鞘相互作用相关的几种分子，包括TAG-1，在发育阶段表达其功能，并在脱髓鞘后的修复中发挥重要作用。

The association between axon-myelin interaction and functional several molecules which are distributed from node of Ranvie to juxtaparanode is well recognized. In this study, we analyzed immunohistochemically the distribution and expression of those molecules, including sodium channel, TAG-1, CNTN1, Caspr and Caspr2, using by teased-fiber preparation in patients with demyelinating neuropathies. The expression of sodium channel in demyelinating neuropathies showed markedly decrease compared with normal control although no morphological changes are observed in light microscopic study. In addition, we confirmed that homologous TAG-1 knockout mice resulted in significant ateliosis. These results may suggest that several molecules which is associated with axon-myelin interaction, including TAG-1, express their function in the development phase and play an important role in repair after demyelination.