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Coenzyme Q10 Depletion in Medical and Neuropsychiatric Disorders: Potential Repercussions and Therapeutic Implications
Open accessAbstract
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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“CoQ10 has been implicated in the pathophysiology of neuro-immune diseases, including MDD [177].”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [177]
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“For example, decreased peripheral levels of CoQ10 have been reported in patients with MDD relative to those measured for controls [177].”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [177]
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“As an antioxidant, CoQ10 protects cells from the damaging effects of reactive oxygen species and reactive nitrogen species [177].”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [177]
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Cognitive remission: a novel objective for the treatment of major depression?
Bortolato, B., Miskowiak, K. W., Köhler, C. A., Maes, M., Fernandes, B. S., Berk, M., & Carvalho, A. F. (2016) · BMC Medicine · doi:10.1186/s12916-016-0560-3 · Cited by 252
Self-citationde Melo, Nunes, S. O. V., Anderson, G., Vargas, H. O., Barbosa, D. S., Gałecki, P., Carvalho, A. F., & Maes, M. H. J. (2017) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2017.04.027 · Cited by 194
Self-citationScaini, G., Rezin, G. T., Carvalho, A. F., STRECK, E. L., Berk, M., & Quevedo, J. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.06.040 · Cited by 187
Self-citationMorris, G., Berk, M., Gałecki, P., Walder, K. R., & Maes, M. H. J. (2015) · Molecular Neurobiology · doi:10.1007/s12035-015-9090-9 · Cited by 163
Self-citationMorris, G., Berk, M., Carvalho, A. F., Maes, M. H. J., Walker, A. J., & Puri, B. K. (2017) · Behavioural Brain Research · doi:10.1016/j.bbr.2017.12.036 · Cited by 155
Self-citation
Metadata
- 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
- Open access
- 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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