The DOI matches its Crossref record; 345 of the 347 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
Coenzyme Q10 for Parkinson's disease
Liu, J., Wang, L., Zhan, S.-Y., & Xia, Y. (2012) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd008150.pub3 · Cited by 32
RetractedAutophagy fights disease through cellular self-digestion
Mizushima, N., Levine, B., Cuervo, A. M., & Klionsky, D. J. (2008) · Nature · doi:10.1038/nature06639 · Cited by 6,452
Metals, Toxicity and Oxidative Stress
Valko, M., Morris, H., & Cronin, M. (2005) · Current Medicinal Chemistry · doi:10.2174/0929867053764635 · Cited by 5,018
Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice
Hara, T., Nakamura, K., Matsui, M., Yamamoto, A., Nakahara, Y., Suzuki-Migishima, R., Yokoyama, M., Mishima, K., Saito, I., Okano, H., et al. (2006) · Nature · doi:10.1038/nature04724 · Cited by 3,882
Loss of autophagy in the central nervous system causes neurodegeneration in mice
Komatsu, M., Waguri, S., Chiba, T., Murata, S., Iwata, J.-I., Tanida, I., Ueno, T., Koike, M., Uchiyama, Y., Kominami, E., et al. (2006) · Nature · doi:10.1038/nature04723 · Cited by 3,500
PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
Narendra, D. P., Jin, S. M., Tanaka, A., Suen, D.-F., Gautier, C. A., Shen, J., Cookson, M. R., & Youle, R. J. (2010) · PLoS Biology · doi:10.1371/journal.pbio.1000298 · Cited by 2,944
PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
Geisler, S., Holmström, K. M., Skujat, D., Fiesel, F. C., Rothfuss, O. C., Kahle, P. J., & Springer, W. (2010) · Nature Cell Biology · doi:10.1038/ncb2012 · Cited by 2,835
Boveris, A., & Chance, B. (1973) · Biochemical Journal · doi:10.1042/bj1340707 · Cited by 2,626
Oxidative stress and neurodegeneration: where are we now?
Halliwell, B. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03907.x · Cited by 2,614
(2012) · The Scientific World JOURNAL · doi:10.1100/tswj · Cited by 2,600
Research works printed but not linked: 3
- Jelin JM, Gregory PJ et al (2009) Natural medicines comprehensive database/compiled by the editors of Pharmacist’s Letter, Prescriber’s Letter, 11th edn. Therapeutic Research Faculty, Stockton, CA, pp 452–457
- Nathan N, Van Konynenburg RA (2009) Treatment study of methylation cycle support in patients with chronic fatigue syndrome and fibromyalgia. 9th International IACFS/ME Conference, Reno, Nevada
- Moreno-Fernández AM, Cordero MD, Garrido-Maraver J, Alcocer-Gómez E, Casas-Barquero N, Carmona-López MI, Sánchez-Alcázar JA, de Miguel M (2012) Oral treatment with amitriptyline induces coenzyme Q deficiency and oxidative stress in psychiatric patients. J Psychiatr Res 46:341–345 · DOI · Paper page
Cited by
Sorted by citations
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
