Mechanistic insights into ubiquinone Q10 in Parkinson’s disease: mitochondrial protection, ferroptosis inhibition, and antioxidant recycling

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Abstract

Background: Parkinson’s disease is a progressive neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra. Although the exact cause of Parkinson’s disease is still unknown, neuroinflammation and mitochondrial dysfunction have been identified as essential factors in the disease’s pathophysiology. Methods: Coenzyme Q10 has gathered considerable attention as a potential therapeutic agent due to its dual function in antioxidant defense and mitochondrial bioenergetics. It is an essential electron carrier in the mitochondrial electron transport chain and plays a crucial role in reducing oxidative stress, a primary cause of neuronal degeneration in Parkinson’s disease. Results: Coenzyme Q10 supplements can enhance mitochondrial activity, reduce oxidative stress, and protect dopaminergic neurons from degeneration. To improve Coenzyme Q10 formulations and ascertain its effectiveness in slowing the progression of Parkinson’s disease, more study is required. Conclusion: This review examines the neuroprotective mechanisms of Coenzyme Q10 and its potential as a therapeutic option for Parkinson’s disease.

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Saadh, M. J., Nazar Saeed, T., Fawzi Al-Hussainy, A., Kyada, A., Ballal, S., Kundlas, M., … Mushtaq, H. (2026). Mechanistic insights into ubiquinone Q10 in Parkinson’s disease: mitochondrial protection, ferroptosis inhibition, and antioxidant recycling. Archives of Physiology and Biochemistry. Taylor and Francis Ltd. https://doi.org/10.1080/13813455.2025.2541698

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