Cited by 96Coenzyme Q10 studies and effectsMitochondrial Function and PathologyParkinson's Disease Mechanisms and Treatments

Coenzyme Q10 Depletion in Medical and Neuropsychiatric Disorders: Potential Repercussions and Therapeutic Implications

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Morris, Gerwyn, Anderson, George, Berk, Michael, Maes, Michael·2013·Molecular Neurobiology

Abstract

Coenzyme Q10 (CoQ10) is an antioxidant, a membrane stabilizer, and a vital cofactor in the mitochondrial electron transport chain, enabling the generation of adenosine triphosphate. It additionally regulates gene expression and apoptosis; is an essential cofactor of uncoupling proteins; and has anti-inflammatory, redox modulatory, and neuroprotective effects. This paper reviews the known physiological role of CoQ10 in cellular metabolism, cell death, differentiation and gene regulation, and examines the potential repercussions of CoQ10 depletion including its role in illnesses such as Parkinson's disease, depression, myalgic encephalomyelitis/chronic fatigue syndrome, and fibromyalgia. CoQ10 depletion may play a role in the pathophysiology of these disorders by modulating cellular processes including hydrogen peroxide formation, gene regulation, cytoprotection, bioenegetic performance, and regulation of cellular metabolism. CoQ10 treatment improves quality of life in patients with Parkinson's disease and may play a role in delaying the progression of that disorder. Administration of CoQ10 has antidepressive effects. CoQ10 treatment significantly reduces fatigue and improves ergonomic performance during exercise and thus may have potential in alleviating the exercise intolerance and exhaustion displayed by people with myalgic encepholamyletis/chronic fatigue syndrome. Administration of CoQ10 improves hyperalgesia and quality of life in patients with fibromyalgia. The evidence base for the effectiveness of treatment with CoQ10 may be explained via its ability to ameliorate oxidative stress and protect mitochondria.

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  8. Morris, G., Anderson, G., Berk, M. & Maes, M. (2013). Coenzyme Q10 Depletion in Medical and Neuropsychiatric Disorders: Potential Repercussions and Therapeutic Implications. MOLECULAR NEUROBIOLOGY, 48 (3), pp.883-903. https://doi.org/10.1007/s12035-013- 8477-8. Persistent Link: http://hdl.handle.net/11343/219793 File Description: Accepted · DOI

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Authors
Morris, G., Anderson, G., Berk, M., & Maes, M.
Affiliations
Deakin University (AU)
Corresponding author
Maes, Michael
Venue
Molecular Neurobiology
Published
2013-06-13
Volume
48
Issue
3
Pages
883-903
ISSN
  • 0893-7648 (ISSN-L)
  • 1559-1182
OpenAlex
W2058368383
Cited by
96
References
347
Citations by year
2026: 3 · 2025: 7 · 2024: 6 · 2023: 6 · 2022: 4 · 2021: 10 · 2020: 11 · 2019: 13 · 2018: 9 · 2017: 7 · 2016: 8 · 2015: 7 · 2014: 3 · 2013: 2
FWCI
0.63
Type
journal article
Language
en
Locations
  • Molecular Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
  • Minerva Access (University of Melbourne) (submittedVersion)
Funders
  • Bristol-Myers Squibb
  • Eli Lilly and Company
  • Pfizer
  • Sanofi
  • Servier
  • H. Lundbeck A/S
  • Cilag
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
coenzyme Q10, Parkinson's disease, depression, chronic fatigue syndrome, fibromyalgia, oxidative stress, mitochondrial dysfunction, neuroprotection, antioxidants, uncoupling proteins, hydrogen peroxide, exercise intolerance, hyperalgesia, mitochondrial electron transport chain, apoptosis, gene expression regulation
MeSH terms
Mental Disorders, Humans, Ubiquinone, Signal Transduction, Nitrosation, Oxidative Stress

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