Damaged neurons in the CNS generally fail to regenerate after
spinal cord injury (SCI), which may be due in part to the formation
of the glial scar, a biochemical and physical barrier against axon
growth. Here we report on evidence for 3 major conclusions. 1)
Antibody-mediated blockade of the growth-inhibitory NG2 molecule
found in glial scars is a viable strategy to promote sensory axon
regeneration. 2) A combinatorial treatment approach that
neutralizes extrinsic inhibition and stimulates intrinsic neuronal
growth capacity is an important strategic consideration because
this method can promote long-distance, anatomically correct axon
regeneration. Accurate growth trajectory is a prerequisite for
functional recovery. 3) After SCI and growth- promoting treatments,
regenerated axons remain chronically demyelinated and exhibit
pathophysiological function, similar to that observed in cases of
multiple sclerosis. This suggests the need for further treatments
designed to restore normal axon conduction after SCI. Overall, a
cure for paralysis after SCI requires that we crudely reproduce
what the developing nervous system does naturally with precision.
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