期刊
NATURE NEUROSCIENCE
卷 22, 期 8, 页码 1269-+出版社
NATURE PORTFOLIO
DOI: 10.1038/s41593-019-0424-1
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资金
- National Institutes of Health (NIH) [NS042291]
- Acorda Therapeutics
- Veterans Administration (Gordon Mansfield Spinal Cord Injury Collaborative Consortium) [IP50RX001045, RRD B7332R, RRD 1I01RX002245]
- NIH [NCRR P51 OD011107-56]
- Craig H. Neilsen Foundation
- Bernard and Anne Spitzer Charitable Trust
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- British Medical Research Council
- Christopher AMP
- Dana Reeve Foundation
- MRC [MR/R004544/1, MR/R004463/1] Funding Source: UKRI
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.
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