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Lookup NU author(s): Emeritus Professor David Mendelow
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2025 by the authors.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.
Author(s): Mantle D, Dewsbury M, Mendelow AD, Hargreaves IP
Publication type: Review
Publication status: Published
Journal: International Journal of Molecular Sciences
Year: 2025
Volume: 26
Issue: 11
Online publication date: 27/05/2025
Acceptance date: 23/05/2025
ISSN (print): 1661-6596
ISSN (electronic): 1422-0067
Publisher: Multidisciplinary Digital Publishing Institute (MDPI)
URL: https://doi.org/10.3390/ijms26115126
DOI: 10.3390/ijms26115126
