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

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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

DOI 10.1007/s12035-013-8477-8

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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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Authors: Morris, G., Anderson, G., Berk, M., & Maes, M.
Affiliations: Deakin University (AU)
Corresponding author: Maes, Michael
ORCID: Morris, Gerwyn
Anderson, George
Maes, Michael
Venue: Molecular Neurobiology
Publisher: Springer Science and Business Media LLC
Published: 2013-06-13
Volume: 48
Issue: 3
Pages: 883-903
ISSN: 0893-7648 (ISSN-L)
1559-1182
DOI: 10.1007/s12035-013-8477-8
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
Open access: green
gateway.webofknowledge.com
Licence: www.springer.com/tdm (tdm)
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 › Clinical 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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Coenzyme Q10 Depletion in Medical and Neuropsychiatric Disorders: Potential Repercussions and Therapeutic Implications

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