Increased cell-free DNA is associated with oxidative damage in patients with schizophrenia

Li, Shuhui; Jiang, Jie; Zhu, Wenli; Wang, Dandan; Dong, Chaoqing; Bu, Yangying; Zhang, Juan; Gao, Daiyutong; Hu, Xiaowen; Wan, Chunling

doi:10.1016/j.jpsychires.2024.04.047

Journal of Psychiatric Research

2024

DOI: 10.1016/j.jpsychires.2024.04.047

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Increased cell-free DNA is associated with oxidative damage in patients with schizophrenia

Shuhui Li,

Jie Jiang,

Wenli Zhu

et al.

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2024

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Cited by 2 publications

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Mitochondrial Dysfunction and Cognitive Impairment in Schizophrenia: The Role of Inflammation

Wang,

Liu,

Fan

et al. 2024

Schizophrenia Bulletin

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Background and Hypothesis The 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 Design Mitochondrial 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 Results Our 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. Conclusions This 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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Mitochondrial Dysfunction and Cognitive Impairment in Schizophrenia: The Role of Inflammation

Wang,

Liu,

Fan

et al. 2024

Schizophrenia Bulletin

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Antioxidants in neuropsychiatric disorder prevention: neuroprotection, synaptic regulation, microglia modulation, and neurotrophic effects

Liu,

Bai,

Tang

et al. 2024

Front. Neurosci.

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Oxidative stress, caused by an imbalance between the generation of reactive oxygen species (ROS) and the body’s intrinsic antioxidant defenses, plays a critical role in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s. Beyond these conditions, recent evidence indicates that dysregulated redox balance is implicated in neuropsychiatric disorders, including schizophrenia, major depressive disorder, and anxiety disorders. Preclinical and clinical studies have demonstrated the potential of antioxidants, such as N-acetylcysteine, sulforaphane, alpha-lipoic acid, L-carnitine, ascorbic acid, selenocompounds, flavones and zinc, in alleviating neuropsychiatric symptoms by mitigating excitotoxicity, enhancing synaptic plasticity, reducing microglial overactivation and promoting synaptogenesis. This review explores the role of oxidative stress in the pathogenesis of neuropsychiatric disorders. It provides an overview of the current evidence on antioxidant therapy’s pharmacological effects, as demonstrated in animal models and clinical studies. It also discusses the underlying mechanisms and future directions for developing antioxidant-based adjuvant therapies. Given the limitations and side effects of existing treatments for neuropsychiatric disorders, antioxidant therapy presents a promising, safer alternative. Further research is essential to deepen our understanding and investigate the clinical efficacy and mechanisms underlying these therapies.

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Increased cell-free DNA is associated with oxidative damage in patients with schizophrenia

Cited by 2 publications

References 56 publications

Mitochondrial Dysfunction and Cognitive Impairment in Schizophrenia: The Role of Inflammation

Mitochondrial Dysfunction and Cognitive Impairment in Schizophrenia: The Role of Inflammation

Antioxidants in neuropsychiatric disorder prevention: neuroprotection, synaptic regulation, microglia modulation, and neurotrophic effects

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