摘要
For decades, numerous investigations have only focused on axon regeneration to restore function after traumatic spinal cord injury （SCI）, as interrupted neuronal pathways have to be reconnected for sensorimotor and autonomic recovery to occur. Experimental approaches have ranged from drug delivery and cell transplantation to genetic manipulations. Certainly, it would be an extraordinary achievement for injured axons to regenerate over long distances, to form synapses with target neurons, and to result in dramatic functional improvement. However, these efforts have been rewarded with limited success to date suggesting that axon regeneration alone may be insufficient to repair compromised functions.
For decades, numerous investigations have only focused on axon regeneration to restore function after traumatic spinal cord injury （SCI）, as interrupted neuronal pathways have to be reconnected for sensorimotor and autonomic recovery to occur. Experimental approaches have ranged from drug delivery and cell transplantation to genetic manipulations. Certainly, it would be an extraordinary achievement for injured axons to regenerate over long distances, to form synapses with target neurons, and to result in dramatic functional improvement. However, these efforts have been rewarded with limited success to date suggesting that axon regeneration alone may be insufficient to repair compromised functions.
基金
supported by the Craig H.Neilsen Foundation(280072)
