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Disease mechanisms in MS

A role for sodium channels in regulation of macrophage-mediated pathology in multiple sclerosis lesions

Nature Reviews Neurology volume 8, page 592 (2012)Cite this article

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In a recent study of brain lesions obtained from patients with multiple sclerosis (MS), researchers have identified a role for the sodium channel Nav1.5 in the phagocytic pathway of myelin degradation by macrophages. Blockade of sodium channels could, therefore, represent a novel therapeutic strategy to attenuate macrophage-mediated CNS destruction.

Joel Black and Stephen Waxman, lead investigators of the study published in the Multiple Sclerosis Journal, had previously demonstrated the expression of sodium channels by immune cells in the brain, including macrophages and microglia, but most of this work was performed in vitro. “It was important for us to examine the expression of sodium channels in situ within tissue obtained from the rapid autopsy of patients with MS, which were provided by our colleague Jia Newcombe,” says Black.

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ORIGINAL RESEARCH PAPER

  1. Black, J. A., Newcombe, J. & Waxman, S. G. Nav1.5 sodium channels in macrophages in multiple sclerosis lesions. Mult. Scler. doi:10.1177/1352458512460417

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  1. Katy Malpass
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Malpass, K. A role for sodium channels in regulation of macrophage-mediated pathology in multiple sclerosis lesions. Nat Rev Neurol 8, 592 (2012). https://doi.org/10.1038/nrneurol.2012.201

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