A current affair in MS

A European team has used the diabetes drug glibenclamide to block inflammation-induced neurodegeneration in mice.1 The team plans to test the nonspecific inhibitor of the cationic channel TRPM4 in an investigator-led clinical trial in multiple sclerosis and is looking for pharmas to develop more specific antagonists of the target.

Transient receptor potential cation channel subfamily M member 4 (TRPM4) is a widely expressed Ca2+-activated, voltage-dependent cation channel that depolarizes the plasma membrane by increasing sodium influx.

A group of German and Swiss researchers hypothesized that TRPM4 might be a key player in MS because disease-associated inflammation leads, in part, to elevated glutamate levels, which promote excitotoxic neurodegeneration by inducing Na+ and Ca2+ influx.2

Indeed, the

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