Expression of oxidative stress-response genes is not activated in the prefrontal cortex of patients with depressive disorder
Abstract
To test the hypothesis that the oxidative stress consistently detected in the peripheral blood of patients with depressive disorder impacts on the functionally relevant brain region, the expression level of nine major genes of the stress response and repair systems has been quantified in the prefrontal cortex of 24 depressive and 12 control subjects. These genes were: superoxide dismutase (SOD1), SOD2, catalase (CAT), gluthatione peroxidase 1 (GPx1), 8-oxoguanine DNA glycosylase (OGG1), nei-like 1 (NEIL1), methionine sulphoxide reductase A (MSRA), telomere repeat-binding factor 2 (TERF2) and C-FOS. Telomere length (a maker of chronic exposure to oxidative stress) has been measured in the DNA of the occipital cortex. No significant difference has been found between the compared groups. It must be concluded that the pathogenic role of the oxidative stress in the cerebral mechanism of depression cannot be inferred from the alteration of peripheral parameters.
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The pathogenic role of oxidative stress in the neurobiology of depression could not be inferred from alterations in the periphery.
“They concluded that the pathogenic role of oxidative stress in the neurobiology of depression could not be inferred from alterations in the periphery [65].”
From Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder (2012) · cites this paper as [65]
Teyssier et al. (2011) demonstrated that the expression of oxidative stress-response genes was not altered in the prefrontal cortex of individuals with MDD.
“Teyssier et al. (2011) demonstrated that the expression of oxidative stress-response genes was not altered in the prefrontal cortex of individuals with MDD.”
From Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder (2012) · cites this paper as [65]
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- Authors
- Teyssier, J.-R., Ragot, S., Chauvet-Gélinier, J.-C., Trojak, B., & Bonin, B.
- Affiliations
- CHU Dijon Bourgogne (FR)
- Venue
- Psychiatry Research
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 186
- Issue
- 2-3
- Pages
- 244-247
- ISSN
- 0165-1781 (ISSN-L)
- OpenAlex
- W1986532380
- Cited by
- 39
- References
- 34
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 3 · 2018: 1 · 2017: 3 · 2016: 3 · 2015: 3 · 2014: 4 · 2013: 2 · 2012: 8
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychiatry Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- oxidative stress, depression, prefrontal cortex, gene expression, superoxide dismutase, catalase, glutathione peroxidase 1, OGG1, NEIL1, MsrA, TRF2, c-fos, telomere length, peripheral blood biomarkers, brain oxidative stress
- MeSH terms
- Adolescent, Adult, Catalase, Child, Child, Preschool, Depression, Female, Glutathione Peroxidase, Humans, Male, Superoxide Dismutase, Proto-Oncogene Proteins c-fos, Prefrontal Cortex, Oxidative Stress, DNA Glycosylases, Methionine Sulfoxide Reductases, Young Adult
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