Cited by 272Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroinflammation and Neurodegeneration Mechanisms

Long-term intracerebral inflammatory response after traumatic brain injury

Gentleman, S.M., Leclercq, P.D., Moyes, L., Graham, D.I., Smith, C., Griffin, W.S.T., Nicoll, J.A.R.·2004·Forensic Science International

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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Crossref · 10.1016/j.forsciint.2004.06.027

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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].”

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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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