Traumatic Brain Injury and Coenzyme Q10: An Overview

TL;DR

This paper reviews how Coenzyme Q10 may help treat traumatic brain injury by supporting mitochondrial function and reducing oxidative stress and inflammation.

Contribution

The paper explores novel therapeutic strategies using CoQ10 for traumatic brain injury, focusing on its mitochondrial and anti-inflammatory roles.

Findings

CoQ10 supports mitochondrial function and reduces oxidative stress and inflammation in TBI.

Animal models show potential for CoQ10 in managing TBI through intranasal delivery.

CoQ10 may prevent cardiovascular complications in TBI patients by improving immune and cardiac function.

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.

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