Long-term intracerebral inflammatory response after traumatic brain injury
Abstract
Epidemiological and pathological studies suggest that head injury is a significant risk factor for subsequent neurodegeneration and cognitive decline in later life. The precise mechanisms for the development of post-traumatic neurodegenerative change are unclear but we hypothesize that persistence of inflammatory processes in the brain may play a key role and that some individuals are more susceptible to such changes based on their genetic make-up. In support of this hypothesis we present evidence of persistent elevated microglial activity in long-term survivors of head injury and the suggestion of an association between the extent of this activity and interleukin-1 genotype.
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TBI is a biphasic injury: after the mechanical primary injury, a secondary dystrophic state produces long-term dysfunction including elevated neuroinflammation due to blood-brain barrier disruption, increased oxidative stress, and persistent changes in the microglial population.
“TBI is a biphasic injury: after the mechanical primary injury, a secondary dystrophic state produces long-term dysfunction in the brain that includes elevated neuroinflammation as a result of blood-brain barrier disruption, increased oxidative stress, and persistent changes in the microglial population [100–106].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [101]
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- Authors
- Gentleman, S. M., Leclercq, P. D., Moyes, L., Graham, D. I., Smith, C., Griffin, W. S. T., & Nicoll, J. A. R.
- Affiliations
- Imperial College London (GB)
- Southern General Hospital (GB)
- Western General Hospital (GB)
- University of Arkansas for Medical Sciences (US)
- Southampton General Hospital (GB)
- Corresponding author
- Gentleman, S.M.
- Venue
- Forensic Science International
- Publisher
- Elsevier BV
- Published
- 2004-12
- Volume
- 146
- Issue
- 2-3
- Pages
- 97-104
- ISSN
- 0379-0738 (ISSN-L)
- OpenAlex
- W2002432434
- Cited by
- 272
- References
- 41
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 14 · 2023: 8 · 2022: 17 · 2021: 17 · 2020: 19 · 2019: 11 · 2018: 14 · 2017: 18 · 2016: 20 · 2015: 19 · 2014: 22 · 2013: 18 · 2012: 16
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Forensic Science International (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG 12411, P01AG012411)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- traumatic brain injury, neuroinflammation, microglial activation, cognitive decline, genetic susceptibility, long-term survivors, chronic inflammation
- MeSH terms
- CD68 Molecule, Adolescent, Adult, Aged, Alleles, Apolipoproteins E, Brain, Brain Injuries, Child, Child, Preschool, Female, Genotype, Humans, Hyperplasia, Hypertrophy, Infant, Inflammation, Interleukin-1, Male, Middle Aged, Phagocytosis, Antigens, Differentiation, Myelomonocytic, Biomarkers, Antigens, CD, Survival Analysis, Case-Control Studies, Macrophage-1 Antigen, Microglia, Forensic Pathology
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