Cited by 1,000Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Inflammation after trauma: Microglial activation and traumatic brain injury

Ramlackhansingh, Anil F., Brooks, David J., Greenwood, Richard J., Bose, Subrata K., Turkheimer, Federico E., Kinnunen, Kirsi M., Gentleman, Steve, Heckemann, Rolf A., Gunanayagam, Karen, Gelosa, Giorgio, Sharp, David J.·2011·Annals of Neurology

DOI 10.1002/ana.22455

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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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Additional file 2 of ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway
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Additional file 4 of Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits
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Additional file 7 of ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway
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Additional file 6 of Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits
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Additional file 6 of ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway
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Additional file 8 of ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway
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Additional file 2 of Anti-acetylated-tau immunotherapy is neuroprotective in tauopathy and brain injury
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Additional file 5 of Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits
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Additional file 1 of Anti-acetylated-tau immunotherapy is neuroprotective in tauopathy and brain injury
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Additional file 9 of ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway
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Additional file 1 of Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits
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Additional file 3 of Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits
Hanscom, M., Loane, D. J., Aubretch, T., Leser, J. M., Molesworth, K., Hedgekar, N., Ritzel, R. M., Abulwerdi, G., Shea‐Donohue, T., & Faden, A. I. (2021) · Figshare · doi:10.6084/m9.figshare.13605616
Additional file 2 of Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits
Hanscom, M., Loane, D. J., Aubretch, T., Leser, J. M., Molesworth, K., Hedgekar, N., Ritzel, R. M., Abulwerdi, G., Shea‐Donohue, T., & Faden, A. I. (2021) · Figshare · doi:10.6084/m9.figshare.13605613
Additional file 4 of Anti-acetylated-tau immunotherapy is neuroprotective in tauopathy and brain injury
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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: Brooks, David J.
Turkheimer, Federico E.
Kinnunen, Kirsi M.
Gentleman, Steve
Heckemann, Rolf A.
Sharp, David J.
Venue: Annals of Neurology
Publisher: Wiley
Published: 2011-06-27
Volume: 70
Issue: 3
Pages: 374-383
ISSN: 0364-5134 (ISSN-L)
1531-8249
DOI: 10.1002/ana.22455
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
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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Inflammation after trauma: Microglial activation and traumatic brain injury

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