Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys
Abstract
Apoptosis is a morphologically defined form of programmed cell death seen in a variety of circumstances, including immune cell selection, carcinogenesis and development. Apoptosis has very recently been seen after ischemic or traumatic injury to the central nervous system (CNS), 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 post-traumatic 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 vitro, it seems likely that chronic demyelination after CNS injury shares features with chronic degenerative disorders like multiple sclerosis.
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Immediately after injury the spinal cord undergoes massive cellular and molecular changes, including increased cell death, infiltration of inflammation cells, axon degeneration, and OL and myelin loss.
“Immediately after injury the spinal cord undergoes massive cellular and molecular changes, including increased cell death [64, 65], infiltration of inflammation cells in the lesion [2–6], axon degeneration [7–10], and OL and myelin loss [13–16, 66, 67].”
From Delayed short-term tamoxifen treatment does not promote remyelination or neuron sparing after spinal cord injury (2020) · cites this paper as [64]
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- Authors
- Crowe, M. J., Bresnahan, J. C., Shuman, S. L., Masters, J. N., & Beattie, M. S.
- Affiliations
- The Ohio State University (US)
- ORCID
- Beattie, Michael S.
- Venue
- Nature Medicine
- Published
- 1997-01
- Volume
- 3
- Issue
- 1
- Pages
- 73-76
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W1982598770
- Cited by
- 1,153
- References
- 0
- Citations by year
- 2026: 8 · 2025: 17 · 2024: 16 · 2023: 10 · 2022: 30 · 2021: 40 · 2020: 23 · 2019: 33 · 2018: 38 · 2017: 44 · 2016: 53 · 2015: 46 · 2014: 59 · 2013: 46 · 2012: 57
- FWCI
- 30.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p50ns010165-25)
- National Institute of Neurological Disorders and Stroke (NS32000, NS-10165, R01NS031193, NS 31193, R01NS032000)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Keywords
- apoptosis, spinal cord injury, secondary degeneration, oligodendrocyte death, demyelination, white matter, programmed cell death, central nervous system injury, cytokines, multiple sclerosis, necrosis, rats, monkeys
- MeSH terms
- Animals, Axons, Cell Nucleus, Contusions, Macaca mulatta, Male, Nerve Degeneration, Neurons, Rats, Inbred Strains, Spinal Cord, Spinal Cord Injuries, Time Factors, Wallerian Degeneration, Apoptosis, Rats, DNA Fragmentation
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