Evidence map›Paper›PMID 38739360›Full record

ReviewAnatomical science international2025

Neuroinflammation and neurodegeneration following traumatic brain injuries.

Matthew Boulton, Ali Al-Rubaie

Abstract readReview
In one paragraph

Review in Anatomical science international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

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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

2 authors.

Matthew BoultonSchool of Health Sciences, Swinburne University of Technology, Hawthorn, VIC, 3122, Australia.
Ali Al-RubaieSchool of Health Sciences, Swinburne University of Technology, Hawthorn, VIC, 3122, Australia. aalrubaie@swin.edu.au.ORCID http://orcid.org/0000-0002-7970-1613

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injuries (TBI) commonly occur following head trauma. TBI may result in short- and long-term complications which may lead to neurodegenerative consequences, including cognitive impairment post-TBI. When investigating the neurodegeneration following TBI, studies have highlighted the role reactive astrocytes have in the neuroinflammation and degeneration process. This review showcases a variety of markers that show reactive astrocyte presence under pathological conditions, including glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3) and S100A10. Astrocyte activation may lead to white-matter inflammation, expressed as white-matter hyperintensities. Other white-matter changes in the brain following TBI include increased cortical thickness in the white matter. This review addresses the gaps in the literature regarding post-mortem human studies focussing on reactive astrocytes, alongside the potential uses of these proteins as markers in the future studies that investigate the proportions of astrocytes in the post-TBI brain has been discussed. This research may benefit future studies that focus on the role reactive astrocytes play in the post-TBI brain and may assist clinicians in managing patients who have suffered TBI.

Indexed as

Brain Injuries, TraumaticNeurodegenerative DiseasesNeuroinflammatory DiseasesAstrocytesBiomarkersBrainGlial Fibrillary Acidic ProteinHumansWhite MatterBiomarkersGlial Fibrillary Acidic ProteinNeurodegenerationNeuroinflammationReactive astrocytesTraumatic brain injury

Identifiers

PMID38739360
PMCPMC11725545

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.