Neuronal and glial apoptosis in human traumatic brain injury
Abstract
To establish reliable methods to aid the timing of brain damage after traumatic brain injury (TBI), brain tissue from 56 autopsy cases with TBI and known survival times, ranging from a few minutes to 126 days, were tested for apoptotic changes to the neuronal and glial cells. Apoptosis was established using the TdT-mediated dUTP nick end labelling (TUNEL) method of in-situ labelling and immunohistochemical reaction of caspase 3. In addition, cellular reaction and astroglial cell differentiation were investigated using histological and immunohistochemical markers. From a survival time of 120 min up to 12 days, TUNEL-positive apoptotic neuronal cells were frequently detected in the contusion zone. The earliest positive caspase 3 reaction in cortical neurons was evident after a posttraumatic interval of 80 min. Detection of apoptotic glial cells using the TUNEL technique showed that as in the case of neuronal cells, the earliest positive TUNEL reaction was obtained after 110 min. In cases of survival times of 120 min up to 4 days, apoptotic glial cells could frequently be detected. However, the first caspase 3-positive glial cells appeared 5 h after injury. Cerebral apoptosis was significantly associated with TBI cases as compared to control cases (P<0.001). The reference histological findings of neutrophilic granulocytes, CD3-positive T-lymphocytes, CD68-positive activated microglial cells/macrophages and TUNEL-positive neuronal cells increases the degree of certainty in determ…
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Chronic neuroinflammation could provoke tau pathology thereby worsening neuronal injury and long-term outcome.
“Together, these studies indicate that chronic neuroinflammation could provoke tau pathology thereby worsening neuronal injury and long-term outcome.”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [154]
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“…of brain injury and hematomas at the site or in the area adjacent to the injury has especially important criminological implications (Bratzke, 2004; Dressler et al., 2007; Hausmann & Betz, 2001; Hausmann et al., 1999; Hausmann et al., 2000; Oehmichen et al., 2003; Takamiya et al., 2007); however,…”
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“78 It commonly occurs in the cortex and hippocampus from 1 dpi up to 2 weeks post injury, based on the severity of injury and model of TBI.”
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“…impedes the neuroinflammation promoted by the accumulated cellular debris and release of pro-inflammatory cytokines; on the other hand, slow or defective clearance of ApoBDs instigates sustained neuroinflammation, which aggravates secondary brain injury and deteriorates clinical outcome [81].”
Histological investigation of amygdala in horned and hornless ewes
Yarar, B., Öztürk, C., Aydın, M. D., & Keleş, O. N. (2026) · Veterinary Research Forum · doi:10.30466/vrf.2024.2038643.4406
“34,35 Neuronal apoptosis to eliminate unnecessary neurons after traumatic injury may be a physiological and protective response to damage, 36 however, premature or impaired apoptosis is observed in the pathological process of many neurodegenerative diseases.”
Tsui, C., Mirkiani, S., Roszko, D. A., Birtle, M. J., DeCorby, A. E., Churchward, M., Mushahwar, V., & Todd, K. G. (2025) · Biomaterials · doi:10.1016/j.biomaterials.2025.123478
Zebrafish аs а Promising Experimental Model of Traumatic Brain Injury
Shevlyakov, A. D., Ilyin, N. P., Galstyan, D., Ikrin, A. N., Kolesnikova, T. O., Apukhtin, K. V., Kotova, M. M., Nikitin, V. S., Amstislavskaya, T. G., Petersen, E. V., et al. (2024) · Российский физиологический журнал им И М Сеченова · doi:10.31857/s0869813924030024
Ilyin, N. P., Galstyan, D., Demin, K., & Kalueff, A. V. (2023) · Journal of Evolutionary Biochemistry and Physiology · doi:10.1134/s0022093023060224
Hunea, I. (2022) · Revista Medico-Chirurgicala · doi:10.22551/msj.2022.03.04
“However, DAI have a particularly negative impact on outcomes, as patients are frequently left with severe motor, cognitive and behavioral impairments (9).”
BackgroundAktas, C., Kanter, M., Uzun, D., & Fidanol, Z. (2011) · doi:10.5835/jecm.v28i3.1009001882
“Our results are in agree- ment with reports of other workers, which suggest that closed head trauma caused apotosis in the frontal cortex (Stone et al., 2002; Lau et al., 2006; Dressler et al., 2007; Kilbourne et al., 2009; Kim et al., 2010).”
Result
- Authors
- Dreßler, J., Hanisch, U., Kuhlisch, E., & Geiger, K. D.
- Affiliations
- Technische Universität Dresden (DE)
- Corresponding author
- Dreßler, J.
- Venue
- International Journal of Legal Medicine
- Published
- 2006-11-15
- Volume
- 121
- Issue
- 5
- Pages
- 365-375
- ISSN
- 0044-3433 (ISSN-L)
- 0937-9827
- 1437-1596
- OpenAlex
- W2006743483
- Cited by
- 94
- References
- 0
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 4 · 2023: 8 · 2022: 5 · 2021: 4 · 2020: 10 · 2019: 6 · 2018: 8 · 2017: 2 · 2016: 2 · 2015: 5 · 2014: 5 · 2013: 3 · 2012: 7
- FWCI
- 1.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- International Journal of Legal Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Autopsy Techniques and Outcomes
- Keywords
- traumatic brain injury, apoptosis, neuronal apoptosis, caspase-3, TUNEL, bruising, postmortem interval estimation, postmortem brain, microglial activation, T cells, forensic neuropathology
- MeSH terms
- CD68 Molecule, Adolescent, Adult, Aged, Aged, 80 and over, Brain, Brain Injuries, Female, Glial Fibrillary Acidic Protein, Humans, Immunohistochemistry, Lymphocytes, Male, Middle Aged, Neuroglia, Neurons, Prospective Studies, Time Factors, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Apoptosis, In Situ Nick-End Labeling, Forensic Pathology, Caspase 3
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