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Oligodendrocytes and Ischemic Brain Injury
Open accessAbstract
Oligodendrocytes, myelin-forming glial cells of the central nervous system, are vulnerable to damage in a variety of neurologic diseases. Much is known of primary myelin injury, which occurs in settings of genetic dysmyelination or demyelinating disease. There is growing awareness that oligodendrocytes are also targets of injury in acute ischemia. Recognition of oligodendrocyte damage in animal models of ischemia requires attention to their distinct histologic features or use of specific immunocytochemical markers. Like neurons, oligodendrocytes are highly sensitive to injury by oxidative stress, excitatory amino acids, trophic factor deprivation, and activation of apoptotic pathways. Understanding mechanisms of oligodendrocyte death may suggest new therapeutic strategies to preserve or restore white matter function and structure after ischemic insults.
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“Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”
From Neurocircuitry of Mood Disorders (2010) · cites this paper as Dewar et al, 2003
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“Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”
From Neurocircuitry of Mood Disorders (2010) · cites this paper as Dewar et al, 2003
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“oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al. 2003; Matute et al. 1997; McDonald et al. 1998).”
From Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression (2008) · cites this paper as Dewar et al. 2003
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Otani, M., Kushida, Y., Kuroda, Y., Wakao, S., Oguma, Y., Sasaki, K., Katahira, S., Terai, R., Ryoke, R., Nonaka, H., et al. (2024) · Stroke and Vascular Neurology · doi:10.1136/svn-2023-002962 · Cited by 2
Laporte, J. P., Akhonda, M. A. B. S., Cortina, L. E., Faulkner, M. E., Gong, Z., Guo, A., Bae, J., Fox, N., Zhang, N., Bergeron, C. M., et al. (2025) · Hypertension Research · doi:10.1038/s41440-025-02114-1 · Cited by 2
White Matter Injury and Potential Treatment in Ischemic Stroke
Song, M., Woodbury, A., & Yu, S. P. (2013) · Springer eBooks · doi:10.1007/978-1-4614-9123-1_2 · Cited by 2
Qiu, C.-W., Sheng, B., & Liu, J. (2012) · Medical Hypotheses · doi:10.1016/j.mehy.2012.09.005 · Cited by 2
Ransom, B. R., Goldberg, M. P., Arai, K., & Baltan, S. (2015) · Elsevier eBooks · doi:10.1016/b978-0-323-29544-4.00009-8 · Cited by 2
Self-citationThe endocannabinoid system as a target for the treatment of neurological disorders
DeMesa, J., Appendino, G., Morello, G., Murray, M. P., & Muñóz, E. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-816475-4.00002-1 · Cited by 2
Oligodendrogenesis After Cerebral Ischaemia and Traumatic Brain Injury
Zhang, Z. G., & Chopp, M. (2013) · EMJ Neurology · doi:10.33590/emjneurol/10314620 · Cited by 2
Sato, T., Matsushima, S., Okumura, M., Maku, T., Kitagawa, T., Tanabe, M., Takatsu, H., Komatsu, T., Sakai, K., Sakuta, K., et al. (2023) · Stroke Vascular and Interventional Neurology · doi:10.1161/svin.123.000995 · Cited by 1
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Wrap it up: myelination of transplanted neurons for repair
Martínez-Reza, M. F., & Götz, M. (2025) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2025.1635551 · Cited by 1
Carreira, R. B., dos Santos, C. C., de Oliveira, J. V. R., Silva, N. N., da Silva, V. D. A., Victor, M. M., Butt, A. M., & Costa, S. L. (2026) · Nutrients · doi:10.3390/nu18071086 · Cited by 1
Sharma, A., Mannan, A., Chitranshi, N., Dua, K., & Singh, T. G. (2026) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2026.104093 · Cited by 1
Zhang, Z., Tan, J., Lv, M., Duan, Z., Wang, C., Gao, M., Cui, Y., & Feng, Y. (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2026.1735477 · Cited by 1
Ferroptosis of microvascular pericytes contributes to ischemia–reperfusion injury in mice
Takaki, H., Nakamura, K., Takashima, M., Ozaki, Y., Yoshino, F., Hidaka, M., Yamanaka, K., Shibahara, T., Kiyohara, T., Wakisaka, Y., et al. (2026) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x261463955 · Cited by 1
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Role of Erythropoietin in Inflammatory Pathologies of the CNS
Ghezzi, P., Bigini, P., & Mengozzi, M. (2006) · Springer eBooks · doi:10.1007/978-0-387-30011-5_12 · Cited by 1
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Metadata
- Authors
- Dewar, D., Underhill, S. M., & Goldberg, M. P.
- Affiliations
- University of Glasgow (GB)
- Washington University in St. Louis (US)
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2003-03
- Volume
- 23
- Issue
- 3
- Pages
- 263-274
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W2077440654
- Cited by
- 335
- References
- 123
- Citations by year
- 2026: 11 · 2025: 11 · 2024: 17 · 2023: 17 · 2022: 14 · 2021: 18 · 2020: 19 · 2019: 20 · 2018: 12 · 2017: 9 · 2016: 24 · 2015: 25 · 2014: 10 · 2013: 23 · 2012: 15
- FWCI
- 6.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- Funders
- National Institutes of Health (5r01ns032626-04)
- Medical Research Council
- National Institute of Neurological Disorders and Stroke (NS 32626, NS36265, R01NS036265)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Keywords
- oligodendrocytes, ischemic brain injury, myelin damage, demyelinating disease, acute cerebral ischemia, oxidative stress, excitatory amino acids, trophic factor deprivation, apoptosis, white matter preservation, immunocytochemical markers
- MeSH terms
- Animals, Brain Ischemia, Humans, Necrosis, Neurotoxins, Oligodendroglia, Apoptosis, Oxidative Stress, Neuroprotective Agents
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