Glutathione deficit impairs myelin maturation: relevance for white matter integrity in schizophrenia patients
Open accessAbstract
Schizophrenia pathophysiology implies both abnormal redox control and dysconnectivity of the prefrontal cortex, partly related to oligodendrocyte and myelin impairments. As oligodendrocytes are highly vulnerable to altered redox state, we investigated the interplay between glutathione and myelin. In control subjects, multimodal brain imaging revealed a positive association between medial prefrontal glutathione levels and both white matter integrity and resting-state functional connectivity along the cingulum bundle. In early psychosis patients, only white matter integrity was correlated with glutathione levels. On the other side, in the prefrontal cortex of peripubertal mice with genetically impaired glutathione synthesis, mature oligodendrocyte numbers, as well as myelin markers, were decreased. At the molecular levels, under glutathione-deficit conditions induced by short hairpin RNA targeting the key glutathione synthesis enzyme, oligodendrocyte progenitors showed a decreased proliferation mediated by an upregulation of Fyn kinase activity, reversed by either the antioxidant N-acetylcysteine or Fyn kinase inhibitors. In addition, oligodendrocyte maturation was impaired. Interestingly, the regulation of Fyn mRNA and protein expression was also impaired in fibroblasts of patients deficient in glutathione synthesis. Thus, glutathione and redox regulation have a critical role in myelination processes and white matter maturation in the prefrontal cortex of rodent and human, a mechanism potentially disrupted in schizophrenia.
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Redox regulation is particularly strong for GRIN2A-containing NMDARs, where a region of the N-terminus is sufficient to mediate the potentiation of currents by reducing agents such as dithiothreitol or GSH.
“Redox regulation is particularly strong for GRIN2A-containing NMDARs, where a region of the N-terminus is sufficient to mediate the potentiation of currents by reducing agents such as Dithiothreitol or GSH 68,69 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [68]
The NMDAR is regulated by redox state: GRIN1 and GRIN2A possess pairs of redox-sensitive cysteine residues whose disulfide bond formation decreases NMDAR currents, while an overlapping group of cysteine residues are subject to inhibitory S-nitrosylation which facilitates disulfide bond formation.
“The NMDAR is regulated by redox state: both GRIN1 and GRIN2A possess pairs of redox-sensitive cysteine residues whose disulfide bond formation decreases NMDAR currents 67,68 , while an overlapping group of cysteine residues are subject to inhibitory Snitrosylation which facilitates disulfide bond formation 67 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [68]
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- Authors
- Monin, A., Baumann, P. S., Griffa, A., Xin, L., Mekle, R., Fournier, M., Butticaz, C., Klaey, M., Cabungcal, J. H., Steullet, P., Ferrari, C., Cuenod, M., Gruetter, R., Thiran, J. P., Hagmann, P., Conus, P., & Do, K. Q.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- École Polytechnique Fédérale de Lausanne (CH)
- Corresponding author
- Do, K Q
- Venue
- Molecular Psychiatry
- Published
- 2014-08-26
- Volume
- 20
- Issue
- 7
- Pages
- 827-838
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- OpenAlex
- W1973349067
- Cited by
- 113
- References
- 75
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 4 · 2023: 7 · 2022: 9 · 2021: 13 · 2020: 4 · 2019: 19 · 2018: 13 · 2017: 9 · 2016: 10 · 2015: 15
- FWCI
- 8.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, other-oa)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- IRIS (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (125759, 310030_135736/1, 320,030_122,419, 130090, 320030)
- Fondation Leenaards
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- glutathione, myelin maturation, white matter integrity, schizophrenia, oligodendrocyte maturation, Fyn, redox regulation, cingulum, resting-state functional connectivity, early psychosis, N-acetylcysteine, prefrontal cortex, myelination
- MeSH terms
- Adult, Animals, Brain, Cells, Cultured, Female, Fibroblasts, Glutamate-Cysteine Ligase, Glutathione, Humans, Male, Myelin Sheath, Oligodendroglia, Schizophrenia, Rats, Wistar, Mice, Knockout, Proto-Oncogene Proteins c-fyn, Young Adult, White Matter
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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 ›
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