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Chondroitinase improves anatomical and functional outcomes after primate spinal cord injury.
Inhibitory extracellular matrices form around mature neurons as perineuronal nets containing chondroitin sulfate proteoglycans that limit axonal sprouting after CNS injury. The enzyme chondroitinase (Chase) degrades inhibitory chondroitin sulfate proteoglycans and improves axonal sprouting and functional recovery after spinal cord injury in rodents. We evaluated the effects of Chase in rhesus monkeys that had undergone C7 spinal cord hemisection. Four weeks after hemisection, we administered multiple intraparenchymal Chase injections below the lesion, targeting spinal cord circuits that control hand function. Hand function improved significantly in Chase-treated monkeys relative to vehicle-injected controls. Moreover, Chase significantly increased corticospinal axon growth and the number of synapses formed by corticospinal terminals in gray matter caudal to the lesion. No detrimental effects were detected. This approach appears to merit clinical translation in spinal cord injury.This work was supported by the National Institutes of Health (NIH, grant no. NS042291 to M.H.T.) and Acorda Therapeutics. Core infrastructure support for the primate spinal cord research facility was provided by the Veterans Administration (Gordon Mansfield Spinal Cord Injury Collaborative Consortium grant nos. IP50RX001045 and RR&D B7332R to M.H.T. and grant no. RR&D 1I01RX002245 to A.R.F.). The California National Primate Research Center is funded by the NIH (grant no. NCRR P51 OD011107-56). Funding was also provided by the Craig H. Neilsen Foundation (M.H.T.), the Bernard and Anne Spitzer Charitable Trust (M.H.T.), the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (M.H.T.), the British Medical Research Council (J.W.F.) and the Christopher & Dana Reeve Foundation (J.W.F.)
Recommended from our members
Chondroitinase improves anatomical and functional outcomes after primate spinal cord injury.
Inhibitory extracellular matrices form around mature neurons as perineuronal nets containing chondroitin sulfate proteoglycans that limit axonal sprouting after CNS injury. The enzyme chondroitinase (Chase) degrades inhibitory chondroitin sulfate proteoglycans and improves axonal sprouting and functional recovery after spinal cord injury in rodents. We evaluated the effects of Chase in rhesus monkeys that had undergone C7 spinal cord hemisection. Four weeks after hemisection, we administered multiple intraparenchymal Chase injections below the lesion, targeting spinal cord circuits that control hand function. Hand function improved significantly in Chase-treated monkeys relative to vehicle-injected controls. Moreover, Chase significantly increased corticospinal axon growth and the number of synapses formed by corticospinal terminals in gray matter caudal to the lesion. No detrimental effects were detected. This approach appears to merit clinical translation in spinal cord injury