Author: ["Maria J. Crowe","Jacqueline C. Bresnahan","Sheri L. Shuman","Jeffery N. Masters","Michael S. Beattie"]
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Abstract
Apoptosis is a morphologically defined form of programmed cell death seen in a variety of circumstances, including immune cell selection, carcinogenesis and development1,2. Apoptosis has very recently been seen after ischemic or traumatic injury to the central nervous system (CNS)3–5, suggesting that active cell death as well as passive necrosis may mediate damage after CNS injury. After spinal cord injury (SCI) in the rat, typical posttraumatic necrosis occurred, but in addition, apoptotic cells were found from 6 hours to 3 weeks after injury, especially in the spinal white matter. Apoptotic cells were positive for oligodendrocyte markers. After SCI in monkeys, apoptotic cells were found within remote degenerating fiber tracts. Both secondary degeneration at the site of SCI and the chronic demyelination of tracts away from the injury appear to be due in part to apoptosis. As cytokines have been shown to mediate oligodendrocyte death in vitro6, it seems likely that chronic demyelination after CNS injury shares features with chronic degenerative disorders like multiple sclerosis.Cite this article
Crowe, M., Bresnahan, J., Shuman, S. et al. Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys. Nat Med 3, 73–76 (1997). https://doi.org/10.1038/nm0197-73 