# Blood–Brain Barrier and Neuronal Model Systems for Studying CoQ10 Metabolism

**Authors:** David Mantle, Neve Cufflin, Mollie Dewsbury, Iain Parry Hargreaves

PMC · DOI: 10.3390/antiox15010041 · Antioxidants · 2025-12-28

## TL;DR

This paper reviews model systems for studying how CoQ10 crosses the blood-brain barrier and affects neuronal metabolism, comparing in vivo and in vitro approaches.

## Contribution

The paper evaluates the suitability of in vitro models over traditional animal models for studying CoQ10 metabolism in the brain.

## Key findings

- In vitro models, especially 3D systems, may better reflect human BBB characteristics than rodent models.
- Model systems can help study CoQ10's role in mitochondrial and lysosomal functions in neurons.
- Interactions between CoQ10, vitamin E, and selenium can be explored using these models.

## Abstract

The disparity in outcomes between preclinical and clinical studies supplementing coenzyme Q10 (CoQ10) in neurological disorders may be a reflection of the differences in the ability of supplemental CoQ10 to access the blood–brain barrier (BBB) in rodents and in humans, which is, in turn, a consequence of contrasting structures of the BBB. The applicability of in vivo animal models to study access of CoQ10 across the BBB and subsequent neuronal metabolism has, therefore, been questioned, and there is an argument, perhaps surprisingly, that in vitro model systems (particularly 3D cellular systems) may be more appropriate. In this article, we have, therefore, reviewed the role of model systems to study the access of CoQ10 across the BBB, as well as the role of such systems in studying the role of CoQ10 in aspects of neuronal metabolism, such as mitochondrial and lysosomal function. In addition, the use of such model systems to study the interactions of CoQ10 with vitamin E and selenium has been reviewed. Finally, the practical application of a neuronal model system to investigate the effect of CoQ10 supplementation on CoQ10 status and mitochondrial metabolism in a CoQ10 deficiency state has been described.

## Linked entities

- **Chemicals:** coenzyme Q10 (PubChem CID 5281915), vitamin E (PubChem CID 14985), selenium (PubChem CID 6326970)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Diseases:** neurological disorders (MESH:D009461)
- **Chemicals:** CoQ10 (MESH:C024989), selenium (MESH:D012643), vitamin E (MESH:D014810)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12837543/full.md

## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12837543/full.md

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Source: https://tomesphere.com/paper/PMC12837543