Cited by 94Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchAutopsy Techniques and Outcomes

Neuronal and glial apoptosis in human traumatic brain injury

Dreßler, J., Hanisch, U., Kuhlisch, E., Geiger, K. D.·2007·International Journal of Legal Medicine

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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Crossref · 10.1007/s00414-006-0126-6

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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.”

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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
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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