Traumatic CNS injuries often cause permanent, devastating disabilities due to a lack of regeneration of damaged axons. Next to an insufficient intrinsic capability of CNS neurons to regrow axons, also inhibitory molecules that are associated with the CNS myelin and the glial scar contribute to the failure of axonal regeneration. Strategies targeting the inhibitory molecules, their receptors or downstream signaling pathways result in little improvement of regeneration in vivo. However, the combination of such approaches together with measures that increase the intrinsic growth potential of neurons reportedly lead to a significantly better outcome. In this mini-review we outline and discuss a novel therapeutic strategy facilitating axon regeneration by directly targeting microtubule dynamics in axonal growth cones and reducing the inhibitory scar formation at the injury site by the anticancer drug Taxol. Moreover, we portray the mechanisms underlying the beneficial effects of Taxol and its potential as an adjuvant drug to accomplish substantial regeneration and functional recovery after CNS injuries in vivo.
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