UC San Diego

Several factors contribute to the lack of repair following spinal cord injury, such as the lack of growth-promoting factors, poor intrinsic central nervous system regeneration abilities, and inhibition due to the glial scar1. The glial scar contains a class of inhibitory extracellular matrix molecules, chondroitin sulfate proteoglycans (CSPGs), which create a physical and chemical barrier to axon regeneration and sprouting. Previous studies showed that administration of an enzyme, chondroitinase ABC (ch'ase), can remove this inhibition

and promote functional and behavioral recovery in smaller animal models. To aid in translation to clinical trials, we examined whether ch'ase administration in a rhesus monkey model of spinal cord injury promoted such recovery. As of now, 9 of the 12 subjects were analyzed and we found a trend towards anatomical and behavioral recovery in ch'ase administered subjects. The trend toward increased corticospinal tract sprouting in ch’ase subjects may demonstrate that the success of ch’ase in smaller animal models is not unfounded. However, the behavioral recovery is not as distinct, and perhaps more optimization of ch’ase treatment is required in the monkey model before translation to clinical trials. Further conclusions can be drawn once the remaining 3 subjects have been analyzed and assessed. However, despite the incomplete dataset and low n, there are interesting trends in the data that may influence whether the ch’ase treatment will move on to clinical trials.