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Ion channels boost axonal injury in multiple sclerosis

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In neuroinflammatory diseases such as multiple sclerosis, ion channels may fan the embers of neurodegeneration. A new study shows that the cation channel TRPM4 (transient receptor potential melastatin 4) crucially contributes to axonal loss in an animal model of multiple sclerosis (pages 1805–1811).

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Figure 1: Simplified view of neurodegenerative mechanisms in demyelinated axons.

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Acknowledgements

I thank K. Ogston for editorial suggestions.

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Authors and Affiliations

  1. Reinhard Hohlfeld is in the Institute of Clinical Neuroimmunology, Ludwig Maximilians University of Munich, and is a member of the Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.,

    Reinhard Hohlfeld

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  1. Reinhard Hohlfeld
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Correspondence to Reinhard Hohlfeld.

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Competing interests

R.H. has received personal compensation for activities such as advisory board service and/or consultancy fees from Teva, Sanofi-Aventis/Genzyme, Bayer, Merck-Serono, Biogen-Idec, Novartis and Morphosys, and has received research grant support from Teva, Bayer, Serono, Biogen-Idec and Novartis.

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Hohlfeld, R. Ion channels boost axonal injury in multiple sclerosis. Nat Med 18, 1743–1745 (2012). https://doi.org/10.1038/nm.3021

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