Evidence mapPaperPMID 40507939Full record

ReviewInternational journal of molecular sciences2025

Traumatic Brain Injury and Coenzyme Q10: An Overview.

David Mantle, Mollie Dewsbury, Alexander David Mendelow, Iain P Hargreaves

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

4 authors.

David MantlePharma Nord (UK) Ltd., Morpeth NE61 2DB, UK.
Mollie DewsburySchool of Pharmacy, Liverpool John Moores University, Liverpool L3 5UA, UK.
Alexander David MendelowNeurosurgical Trials Group, University of Newcastle upon Tyne, Newcastle upon Tyne NE1 7RU, UK.ORCID 0000-0002-9717-3164
Iain P HargreavesSchool of Pharmacy, Liverpool John Moores University, Liverpool L3 5UA, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of morbidity and mortality in patients who have suffered traumatic brain injury (TBI) is such that novel therapeutic strategies are currently required. There is good evidence that ischaemia is the primary, and sometimes the secondary, cause of brain damage in TBI. This ischaemia may lead to mitochondrial dysfunction, with associated oxidative stress and inflammation, in the pathogenesis of brain injury following head trauma. This, in turn, provides a rationale for the use of supplemental coenzyme Q10 (CoQ10) in the management of TBI, given its key roles in normal mitochondrial function and as an antioxidant and anti-inflammatory agent. In this article, we, therefore, review the use of supplemental CoQ10 in animal models of TBI and its potential application in the management of TBI patients. The problem of blood-brain barrier access is discussed, and how this might be circumvented via the use of an intranasal route to provide direct access of CoQ10 to the brain. In addition, there is evidence that TBI patients have an increased risk of developing cardiac dysfunction and that this may be mediated by aberrant immune action. Given the role of CoQ10 in promoting normal cardiac function and normal immune function, the administration of CoQ10 to prevent cardiovascular complications may improve outcomes in TBI patients.

Indexed as

Brain Injuries, TraumaticUbiquinoneAnimalsAntioxidantsBlood-Brain BarrierHumansMitochondriaOxidative StressAntioxidantscoenzyme Q10Ubiquinonecoenzyme Q10intranasal drug deliverymitochondrial dysfunctionoxidative stresstraumatic brain injury (TBI)

Identifiers

PMID40507939
PMCPMC12154391

What Socratic holds

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Registered trials

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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.