The DOI matches its Crossref record; 92 of the 93 references it cites were found in a registry or an index.
Chapter 4 Cell death in models of spinal cord injury
Abstract
Current treatments for acute spinal cord injury are based on animal models of human spinal cord injury (SCI). These models have shown that the initial traumatic injury to cord tissue is followed by a long period of secondary injury that includes a number of cellular and biochemical cascades. These secondary injury processes are potential targets for therapies. Continued refinement of rat and mouse models of SCI, along with more detailed analyses of the biology of the lesion in these models, points to both necrotic and apoptotic mechanisms of cell death after SCI. In this chapter, we review recent evidence for long-term apoptotic death of oligodendrocytes in long tracts undergoing Wallerian degeneration following SCI. This process appears to be related closely to activation of microglial cells. It is has been thought that microglial cells might be the source of cytotoxic cytokines, such as tumor necrosis factor-alpha (TNF-alpha), that kill oligodendrocytes. However, more recent evidence in vivo suggests that TNF-alpha by itself may not induce necrosis or apoptosis in oligodendrocytes. We review data that suggests other possible pathways for apoptosis, such as the neurotrophin receptor p75 which is expressed in both neurons and oligodendrocytes after SCI in rats and mice. In addition, it appears that microglial activation and TNF-alpha may be important in acute SCI. Ninety minutes after a moderate contusion lesion, microglia are activated and surround dying neurons. In an 'atraumatic' model of SCI, we have now shown that TNF-alpha appears to greatly potentiate cell death mediated by glutamate receptors. These studies emphasize that multiple mechanisms and interactions contribute to secondary injury after SCI. Continued study of both contusion models and other new approaches to studying these mechanisms will be needed to maximize strategies for acute and chronic therapies, and for neural repair.
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“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 [65]
Citations
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Traumatic Spinal Cord Injury: An Overview of Pathophysiology, Models and Acute Injury Mechanisms
Alizadeh, A., Dyck, S. M., & Karimi‐Abdolrezaee, S. (2019) · Frontiers in Neurology · doi:10.3389/fneur.2019.00282 · Cited by 1,509
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Hausmann, O. N. (2003) · Spinal Cord · doi:10.1038/sj.sc.3101483 · Cited by 622
Degenerative and regenerative mechanisms governing spinal cord injury
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Metadata
- Authors
- Beattie, M. S., Hermann, G. E., Rogers, R. C., & Bresnahan, J. C.
- Affiliations
- The Ohio State University Wexner Medical Center (US)
- Corresponding author
- Beattie, Michael S.
- Venue
- Progress in Brain Research
- Publisher
- Elsevier
- Published
- 2002
- Volume
- 137
- Pages
- 37-47
- ISSN
- 0079-6123 (ISSN-L)
- OpenAlex
- W1527455107
- Cited by
- 453
- References
- 93
- Citations by year
- 2026: 5 · 2025: 15 · 2024: 15 · 2023: 16 · 2022: 20 · 2021: 16 · 2020: 23 · 2019: 30 · 2018: 18 · 2017: 17 · 2016: 22 · 2015: 38 · 2014: 23 · 2013: 17 · 2012: 21
- FWCI
- 38.08
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Progress in brain research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ohio State University
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-52142, R01DK052142)
- National Institute of Neurological Disorders and Stroke (NS38079, R01NS038079)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Spinal Cord Injury Research
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- spinal cord injury, secondary injury, cell death, apoptosis, necrosis, oligodendrocytes, Wallerian degeneration, microglial activation, TNF-α, glutamate receptors, bruising, animal models of spinal cord injury
- MeSH terms
- Animals, Disease Models, Animal, Necrosis, Oligodendroglia, Spinal Cord Injuries, Time Factors, Cell Death, Apoptosis, Disease Progression, Rats
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