The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Inflammation after trauma: Microglial activation and traumatic brain injury
Abstract
Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function. Methods: Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered. Results: PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage. Interpretation: We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed. ANN NEUROL 2011;
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“and imaging studies showing increased binding of PK-[11C](R)PK11195 ligand, expressed by activated microglia, between 11 months and 17 years post-injury (86).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [86]
In the citing paper
“Additionally, TBIs and head traumas are associated with neuroinflammation, which can persist for decades following the initial incident [51,52,53].”
From Head Injury and Amyotrophic Lateral Sclerosis: Population-Based Study from the National ALS Registry (2025) · cites this paper as [52]
In the citing paper
“Since the impacts of a severe head injury can be sustained for years after the incident, the effects of a head injury received at a younger age may not appear until later stages of life [51,52,53].”
From Head Injury and Amyotrophic Lateral Sclerosis: Population-Based Study from the National ALS Registry (2025) · cites this paper as [52]
In the citing paper
“In human patients, increased microglial activation is even detectable by PET scan 17 years after the primary injury [114].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [114]
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Metadata
- Authors
- Ramlackhansingh, A. F., Brooks, D. J., Greenwood, R. J., Bose, S. K., Turkheimer, F. E., Kinnunen, K. M., Gentleman, S., Heckemann, R. A., Gunanayagam, K., Gelosa, G., & Sharp, D. J.
- Affiliations
- Hammersmith Hospital (GB)
- UCL Queen Square Institute of Neurology (GB)
- Goldsmiths University of London (GB)
- Corresponding author
- Sharp, David J.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2011-06-27
- Volume
- 70
- Issue
- 3
- Pages
- 374-383
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2096019298
- Cited by
- 999
- References
- 32
- Citations by year
- 2026: 40 · 2025: 57 · 2024: 60 · 2023: 62 · 2022: 71 · 2021: 104 · 2020: 92 · 2019: 86 · 2018: 66 · 2017: 71 · 2016: 71 · 2015: 75 · 2014: 58 · 2013: 49 · 2012: 31
- FWCI
- 28.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Imperial College Healthcare Charity
- Dunhill Medical Trust
- Medical Research Council
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- traumatic brain injury, microglial activation, neuroinflammation, [11C]PK11195 PET, thalamus, cognitive impairment, subcortical structures, diffusion tensor imaging, structural brain abnormalities
- MeSH terms
- Adult, Amnesia, Brain Injuries, Cognition Disorders, Educational Status, Female, Humans, Image Processing, Computer-Assisted, Inflammation, Isoquinolines, Macrophage Activation, Magnetic Resonance Imaging, Male, Memory, Middle Aged, Neuropsychological Tests, Thalamus, Wechsler Scales, Glasgow Coma Scale, Cluster Analysis, Microglia, Positron-Emission Tomography, Diffusion Tensor Imaging, Executive Function
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