Experts review the evidence on coenzyme Q10 and cognitive decline

By Tarun Sai LomteReviewed by Susha Cheriyedath, M.Sc.Sep 9 2025

Animal studies suggest CoQ10 protects memory and learning, but human evidence remains inconsistent, highlighting the urgent need for rigorous trials to determine its role in preventing cognitive decline.

Coenzyme Q10 and Cognition: A Review. Image Credit: Svetlyachock / Shutterstock

In a recent study published in the journal Nutrients, Australian researchers reviewed the effects of coenzyme Q10 (CoQ10) supplementation on cognition. Approximately 22% of the world’s population is estimated to be 60 years or older by 2050. Accompanying this change will be an increase in people with cognitive decline and the prevalence of neurodegenerative diseases. The causes of neurodegenerative diseases and cognitive decline are multifactorial, but the major contributors are oxidative stress, inflammation, poor cardiovascular health, decreased cerebral blood flow, and mitochondrial dysfunction.

These multiple processes in the body and brain require various targeted therapeutic approaches. Various approaches to addressing age-related cognitive decline have been employed, including dietary modifications, physical activity, medications, and nutritional supplements. CoQ10 is an antioxidant and metabolic stimulant that positively influences biological mechanisms relevant to cognition, with mixed effects on cognitive test performance in trials. In the present study, researchers reviewed the effects of CoQ10 supplementation on cognition.

Cardiovascular and non-cognitive effects of CoQ10

CoQ10 plays a major role in adenosine triphosphate (ATP) synthesis by transporting electrons from Complexes I and II to Complex III in the electron transport chain. Its bioavailability differs between formulations such as ubiquinone and ubiquinol, which may influence clinical outcomes. In a clinical trial, preoperative CoQ10 therapy in patients scheduled for an elective heart surgery increased cardiac and myocardial mitochondrial CoQ10 levels, improving the efficiency of energy production.

A meta-analysis of trials of CoQ10 treatment in heart failure indicated that CoQ10 supplementation enhanced ejection fraction by 3.67% and reduced the New York Heart Association (NYHA) functional class by 0.3. A study reported that long-term CoQ10 therapy was safe, alleviated symptoms, and reduced adverse cardiovascular events in patients with chronic heart failure.

Evidence from in vitro and animal studies

A study in mice investigated whether CoQ10 supplementation slows age-related cognitive decline compared to a regular diet. Although no significant performance improvements were observed in a test measuring learning and spatial memory, CoQ10 levels were significantly elevated within the cortex. Another study examined the combined effects of CoQ10 and vitamin E, and found benefits of the combination treatment on learning in aged mice.

In a rat model of Alzheimer’s disease (AD), CoQ10 therapy improved memory, retention, and learning, with substantial decreases in oxidative stress and increases in ATP levels within the cerebral cortex and hippocampus. Moreover, another study reported improved learning and memory with CoQ10 treatment in rats with cognitive dysfunction.

One study examined the relationship between AD and CoQ10 in genetically modified mice and found that CoQ10 administration altered the expression of 12 proteins in the hippocampus and improved spatial memory in genetically modified mice with AD. Specifically, the overexpression of complexin 1 (CPLX-1) and CPLX-2 following CoQ10 therapy prevented memory impairments.

Furthermore, CoQ10 therapy significantly improved cognitive functions in a double-transgenic mouse model, preventing AD progression through decreased inflammation and oxidative stress, as well as the activation of autophagy. CoQ10 supplementation improved short-term memory impairments in a rat model of Parkinson’s disease, and the effect was further enhanced in combination with wheatgrass, sesamol, and thymol.

Evidence from clinical research

Research on the cognitive effects of CoQ10 supplements in healthy people is limited, with only two randomized clinical trials (RCTs) conducted to date. One trial assessed the impact of a low-dose CoQ10 in combination with mineral and multivitamin supplements in healthy females. Cerebral blood flow was significantly increased during cognitive tasks in the treatment group, albeit task performance showed no changes.

The other trial found no significant differences in the digit symbol substitution test, the trail making test, and the memory performance index (MPI) in people taking ubiquinol (reduced form of CoQ10). Notably, people who were cognitively normal at baseline showed significant improvements in MPI following 34 weeks of ubiquinol supplementation. The review emphasized that these findings should be interpreted cautiously due to dose, formulation, and statistical limitations. In AD, CoQ10 treatment had no detectable effects on cerebrospinal fluid biomarkers, suggesting no effects on cognition.

In individuals with mild cognitive impairment, a one-year supplementation with ubiquinol improved cerebral vasoreactivity and reduced inflammation in males, with no changes in cognition observed in either sex. Furthermore, RCTs of the combined CoQ10 and vitamin E treatment reported no improvements in cognitive function in patients with Parkinson’s disease.

One study reported that CoQ10 supplementation improved cognitive function, reduced fatigue symptoms, enhanced working memory, and improved arithmetic task performance in patients with chronic fatigue syndrome. In a study of patients with progressive supranuclear palsy, CoQ10 administration improved cognitive tasks involving the frontal lobe.

Concluding remarks

In summary, while animal studies suggest protective effects of CoQ10 on cognition in healthy aging and neurodegenerative disease models, clinical trials demonstrate some benefits in specific disease contexts but not in healthy aging, with several studies reporting non-significant or null effects. These null effects may be attributed to insufficient statistical power and small sample sizes rather than the absence of an effect. However, the overall mixed findings underscore the need for high-quality clinical trials.