Impaired axonal transport is implicated in the pathogenesis of many neurodegenerative diseases; but its potential role in the neuroinflammatory disease multiple sclerosis has not been determined. Using in vivo two-photon imaging, Sorbara et al. found widespread deficits in both anterograde and retrograde transport in acute and chronic mouse models of multiple sclerosis. These defects occurred even in 'normal'-appearing axons, suggesting that axonal transport deficits are an early event in disease pathogenesis. The defects were reversed by treatment with anti-inflammatory drugs or redox scavengers, suggesting that they might be a suitable target for therapeutic strategies.
Sorbara, C. D. et al. Pervasive axonal transport deficits in multiple sclerosis models. Neuron http://dx.doi.org/10.1016/j.neuron.2014.11.006 (2014)
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Whalley, K. Transport disruption in multiple sclerosis. Nat Rev Neurosci 16, 2 (2015). https://doi.org/10.1038/nrn3892