RESUMO
Trauma in the adult mammalian central nervous system (CNS) has devastating clinical consequences due to the failure of injured axons to spontaneously regenerate. Over 20 years ago, pioneering work demonstrated that the non-permissive nature of CNS myelin for axon outgrowth contributes to this regenerative failure. Over the past few years, tremendous progress has been made in our understanding of the inhibitory components of CNS myelin, the axonal receptors that respond to these cues, and the intracellular signaling cascades mediating axon outgrowth inhibition. Several approaches designed to antagonize molecular mediators of axon inhibition have been tested in an effort to promote regenerative growth after CNS injury. These studies have validated the role of many candidate proteins in axon outgrowth inhibition; however, other approaches such as the generation of knockout mice for myelin-associated inhibitors have created new questions in the field.
