Electrophysiological intermediate biomarkers for oxidative stress in schizophrenia
Open accessAbstract
Objective Diverse electrophysiological abnormalities have been associated with schizophrenia, but the underlying causes remain elusive. We tested whether the altered oxidative stress in schizophrenia contributes to the electrophysiological abnormalities.Methods We used an auditory oddball task to measure mismatch negativity (MMN) and gamma band response on 29 schizophrenia patients and 25 normal controls. Oxidative stress was assessed by monomeric glutathione (GSH, reduced form) and glutathione disulfide (GSSG, oxidized form).Results Patients had reduced MMN (p=0.015) and reduced power of gamma band responses at 21-40 Hz and 41-85 Hz (all p<0.001). GSH was significantly lower (p<0.001) while %GSSG was higher (p=0.023) in patients compared with controls. MMN was correlated with GSH in controls; while 21-40 Hz responses were correlated with GSH in patients. Lower GSH and higher GSSG levels were associated with low community functioning (p=0.018). Multivariate mediation modeling showed that gamma band at 21-40 Hz was a significant mediator for GSH effect on community functions.Conclusions High beta/low gamma range (21-40 Hz) responses may be an intermediate biomarker indexing oxidative stress and its effect on clinical functions.Significance Electrophysiological abnormalities and associated clinical functional changes may in part be associated with heightened oxidative stress in schizophrenia.
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The power of beta/gamma neuronal activity is positively correlated with blood glutathione levels in patients.
“Interestingly, the power of β/γ neuronal activity is positively correlated with blood GSH levels in patients (Ballesteros et al., 2013).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Ballesteros et al., 2013
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- Authors
- Ballesteros, A., Summerfelt, A., Du, X., Jiang, P., Chiappelli, J., Tagamets, M., O’Donnell, P., Kochunov, P., & Hong, L. E.
- Affiliations
- University of Maryland, Baltimore (US)
- Corresponding author
- Hong, L. Elliot
- ORCID
- Venue
- Clinical Neurophysiology
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 124
- Issue
- 11
- Pages
- 2209-2215
- ISSN
- 1388-2457 (ISSN-L)
- PMC
- PMC4030436
- OpenAlex
- W2053937596
- Cited by
- 34
- References
- 63
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 3 · 2018: 1 · 2017: 3 · 2016: 1 · 2015: 5 · 2014: 6 · 2013: 1
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01MH085646, R01DA027680, R21DA033817)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Social Sciences › Arts and Humanities › Philosophy › Mental Health and Psychiatry
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- schizophrenia, oxidative stress, glutathione, glutathione disulfide, mismatch negativity, gamma-band responses, auditory oddball paradigm, intermediate biomarkers, community functioning, mediation analysis
- MeSH terms
- Adult, Analysis of Variance, Evoked Potentials, Female, Glutathione, Humans, Male, Models, Biological, Oxidation-Reduction, Schizophrenia, Biomarkers, Oxidative Stress, Glutathione Disulfide
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