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Ion channels boost axonal injury in multiple sclerosis

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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I thank K. Ogston for editorial suggestions.

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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).

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