SynthesisSchizophrenia bulletin2025
Mitochondrial Dysfunction and Cognitive Impairment in Schizophrenia: The Role of Inflammation.
Synthesis in Schizophrenia bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Schizophrenia: Converging Neurobiological Mechanisms and Emerging Therapeutic Strategies.Biomolecules · 2026Review
- Modulation of mitochondrial DNA copy number: therapeutic potential of phytochemicals and plant extracts-a comprehensive review.Archives of pharmacal research · 2026Review
- Metformin-associated lactic acidosis in an elderly diabetic patient without classical risk factors: a case report.Therapeutic advances in drug safety · 2026Article
- Association Between Frontotemporal Atrophy and Cognitive Impairment in Patients with Schizophrenia Based on Computed Tomography Imaging.Neuropsychiatric disease and treatment · 2026Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors.
Funding
Abstract
background and hypothesisThe complex immune-brain interactions and the regulatory role of mitochondria in the immune response suggest that mitochondrial damage reported in schizophrenia (SZ) may be related to abnormalities observed in immune and brain functions. STUDY
designMitochondrial DNA copy number (mtDNA CN), a biomarker of mitochondrial function, was assessed in peripheral blood leukocytes (PBLs) of 121 healthy individuals and 118 SZ patients before and after 8 weeks of antipsychotic treatment, and a meta-analysis related to blood mtDNA CN was conducted. Plasma C-reactive protein (CRP) levels in SZ patients were obtained from the medical record system. Spearman correlation analysis and hierarchical linear regression were used to analyze the relationships among mtDNA CN, CRP levels, and cognitive function. A mediation model was constructed using the PROCESS program. STUDY
resultsOur results revealed the decreased mtDNA CN in PBLs from SZ patients (P = .05). The meta-analysis supported the decreased blood mtDNA CN in SZ patients (P < .01). The mtDNA CN in PBL was positively correlated with working memory (P = .02) and negatively correlated with plasma CRP levels (P = .039). Furthermore, a lower mtDNA CN in PBL in SZ patients was a significant predictor of worse working memory (P = .006). CRP acted as a mediator with an 8.0% effect.
conclusionsThis study revealed an association between peripheral mitochondrial dysfunction and cognitive impairment in SZ, with inflammation acting as a mediating effect. Therefore, mitochondrial dysfunction might provide novel targets for new treatments for cognitive impairment in SZ.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.