Mitochondrial dysfunction, oxidative stress, and major depressive disorder
Open accessAbstract
There is controversy about depression being a physical illness, in part because a reproducible, sensitive, and specific biologic marker is not available. However, there is evidence that mitochondrial dysfunction and oxidative stress may be associated with abnormal brain function and mood disorders, such as depression. This paper reviews selected human and animal studies providing evidence that intracellular mitochondrial metabolic dysfunction in specific brain regions is associated with major depressive disorder. This supports the hypothesis that chronic mitochondrial dysfunction in specific tissues may be associated with depression. Evaluation of mitochondrial dysfunction in specific tissues may broaden the perspective of depression beyond theories about neurotransmitters or receptor sites, and may explain the persistent signs and symptoms of depression.
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Changes in mitochondrial DNA and cell membrane permeability were found in both depression patients and animal models of depression.
“Changes in mitochondrial DNA and cell membrane permeability were found in both depression patients and animal models of depression [32, 33].”
From APOE4 genotype exacerbates the depression-like behavior of mice during aging through ATP decline (2021) · cites this paper as [32]
The Animal studies section reports mtDNA defects in many patients with mood disorder and describes changes in mitochondrial membrane permeability in rats. But the rat experiment was a model of epilepsy, not depression, and the passage concerns a mitochondrial membrane rather than cell membrane permeability. The paper therefore does not establish both changes in both depression patients and animal models of depression. (LLM, conf=0.84)
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- Authors
- Tobe, E.
- Affiliations
- Cooper Medical School of Rowan University (US)
- Corresponding author
- Tobe, Edward
- Venue
- Neuropsychiatric Disease and Treatment
- Publisher
- Informa UK Limited
- Published
- 2013-04
- Volume
- 9
- Pages
- 567
- ISSN
- 1176-6328 (ISSN-L)
- PMC
- PMC3640606
- OpenAlex
- W2038183514
- Cited by
- 156
- References
- 5
- Citations by year
- 2026: 16 · 2025: 10 · 2024: 13 · 2023: 14 · 2022: 8 · 2021: 13 · 2020: 6 · 2019: 10 · 2018: 14 · 2017: 18 · 2016: 12 · 2015: 14 · 2014: 5 · 2013: 3
- FWCI
- 7.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Neuropsychiatric Disease and Treatment (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- mitochondrial dysfunction, oxidative stress, major depressive disorder, depression, brain metabolism, mood disorders, biomarkers
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