Evidence map›Paper›PMID 23231074›Full record

ArticleNeuropathology and applied neurobiology2013

The neuroinflammatory response in humans after traumatic brain injury.

C Smith, S M Gentleman, P D Leclercq, L S Murray, W S T Griffin, D I Graham, J A R Nicoll

Open access · greenAbstract read
In one paragraph

Article in Neuropathology and applied neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 2 pooled it
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

110 citing papers in PubMed, 2 syntheses or guidelines pooled it, 217 citations in OpenAlex.

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  8. ALKBH5 demethylates the mProceedings of the National Academy of Sciences of the United States of America · 2025
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50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

C SmithAcademic Dept. of Neuropathology, University of Edinburgh, Edinburgh, UK; University Academic Dept. of Neuropathology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK.
S M Gentleman
P D Leclercq
L S Murray
W S T Griffin
D I Graham
J A R Nicoll
Southern General Hospital · GBCharing Cross Hospital · GBCentral Arkansas Veterans Healthcare System · USSouthampton General Hospital · GB

Funding

THE APOE-APP AXIS IN ALZHEIMER PATHOGENESISP01AG012411 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI GRIFFIN, SUE TILTON · 1995 to 2020
$25.0M
NIA NIH HHS AG12411NIA NIH HHS P01 AG012411
6 · The paper itself

Abstract

aimsTraumatic brain injury is a significant cause of morbidity and mortality worldwide. An epidemiological association between head injury and long-term cognitive decline has been described for many years and recent clinical studies have highlighted functional impairment within 12 months of a mild head injury. In addition chronic traumatic encephalopathy is a recently described condition in cases of repetitive head injury. There are shared mechanisms between traumatic brain injury and Alzheimer's disease, and it has been hypothesized that neuroinflammation, in the form of microglial activation, may be a mechanism underlying chronic neurodegenerative processes after traumatic brain injury.

methodsThis study assessed the microglial reaction after head injury in a range of ages and survival periods, from <24-h survival through to 47-year survival. Immunohistochemistry for reactive microglia (CD68 and CR3/43) was performed on human autopsy brain tissue and assessed 'blind' by quantitative image analysis. Head injury cases were compared with age matched controls, and within the traumatic brain injury group cases with diffuse traumatic axonal injury were compared with cases without diffuse traumatic axonal injury.

resultsA major finding was a neuroinflammatory response that develops within the first week and persists for several months after traumatic brain injury, but has returned to control levels after several years. In cases with diffuse traumatic axonal injury the microglial reaction is particularly pronounced in the white matter.

conclusionsThese results demonstrate that prolonged microglial activation is a feature of traumatic brain injury, but that the neuroinflammatory response returns to control levels after several years.

Indexed as

AdolescentAdultAgedAge FactorsBrainBrain InjuriesHumansInflammationMicrogliaMiddle AgedYoung Adultmicroglianeuroinflammationneurotraumatraumatic axonal injury

Identifiers

PMID23231074
PMCPMC3833642
OpenAlexW2131211125

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.