Oxidative Stress in Schizophrenia

Bošković, Marija; Vovk, Tomaž; B, Kores Plesničar; Grabnar, Iztok

doi:10.2174/157015911795596595

Cited by 205 publications

(81 citation statements)

References 62 publications

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“…For example, an impaired capacity to synthesize glutathione, an important antioxidant component, due to genetic polymorphism is a vulnerability factors for schizophrenia (Gysin et al 2007). Also, study in schizophrenia patients showed a positive association between schizophrenia and a functional polymorphism in the gene for manganese SOD (Boskovic et al 2011). On the other hand, environmental factors such as psychosocial and oxidative stress play an important role in the onset and progression of these diseases.…”

Section: Discussionmentioning

confidence: 99%

“…As such, oxidative DNA damage has been proposed as culprits in the most recent hypotheses concerning the pathophysiology of schizophrenia and its associated symptoms (Zhang et al 2010). This alteration has been recognized in treated, untreated and early-stage schizophrenic patients (Boskovic et al 2011). For example, a higher level of 8-oxodG in the blood has been reported in non-remission schizophrenia patients (Sertan Copoglu et al 2015).…”

Section: Dna Damage In Schizophreniamentioning

confidence: 98%

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DNA Damage in Major Psychiatric Diseases

et al. 2016

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Human cells are exposed to exogenous insults and continuous production of different metabolites. These insults and unwanted metabolic products might interfere with the stability of genomic DNA. Recently many studies demonstrated that different psychiatric disorders show substantially high level of oxidative DNA damage in the brain accompanied with morphological and functional alterations. It reveals that damaged genomic DNA may contribute to the pathophysiology of these mental illnesses. Here we review the role of oxidative damage and reduced antioxidant ability in some vastly studied psychiatric disorders and emphasize the inclusion of treatment options involving DNA repair. In addition, while most currently used antidepressants are based on the manipulation of the neurotransmitter regulation in managing different mental abnormalities, they are able to prevent or reverse neurotoxin-induced DNA damage. Therefore, it may be plausible to target on genomic DNA alterations for psychiatric therapies, which is of pivotal importance for future anti-psychiatric drug development.

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Section: Discussionmentioning

confidence: 99%

Section: Dna Damage In Schizophreniamentioning

confidence: 98%

DNA Damage in Major Psychiatric Diseases

et al. 2016

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“…In this regard, molecules with antioxidant activity (like melatonin, lipoic acid, coenzyme Q10, vitamin E, vitamin C, N -acetyl cysteine, and others) may be beneficial as a supplementary treatment in WD (Boškovic et al 2011). Future studies aimed to evaluate the possible usefulness of antioxidants as a supplemental therapy in this disease are warranted.…”

Section: Discussionmentioning

confidence: 99%

Treatment with d-penicillamine or zinc sulphate affects copper metabolism and improves but not normalizes antioxidant capacity parameters in Wilson disease

et al. 2013

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Copper accumulation in tissues due to a biallelic pathogenic mutation of the gene: ATP7B results in a clinical phenotype known as Wilson disease (WD). Aberrations in copper homeostasis can create favourable conditions for superoxide-yielding redox cycling and oxidative tissue damage. Drugs used in WD treatment aim to remove accumulated copper and normalise the free copper concentration in the blood. In the current study the effect of decoppering treatment on copper metabolism and systemic antioxidant capacity parameters was analyzed. Treatment naïve WD patients (TNWD) (n = 33), those treated with anti-copper drugs (TWD) (n = 99), and healthy controls (n = 99) were studied. Both TNWD and TWD patients characterised with decreased copper metabolism parameters, as well as decreased total antioxidant potential (AOP), glutathione (GSH) level, activity of catalase, glutathione peroxidase (GPx), and S-transferase glutathione, compared to controls. TWD patients had significantly lower copper metabolism parameters, higher total AOP and higher levels of GSH than TWD individuals; however, no difference was observed between these two patient groups with respect to the rest of the antioxidant capacity parameters. Patients who had undergone treatment with d-penicillamine or zinc sulphate did not differ with respect to copper metabolism or antioxidant capacity parameters, with the exception of GPx that was lower in d-penicillamine treated individuals. These data suggest that anti-copper treatment affects copper metabolism as well as improves, but does not normalize, natural antioxidant capacity in patients with WD. We propose to undertake studies aimed to evaluate the usefulness of antioxidants as well as selenium as a supplemental therapy in WD.

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“…Nishioka and Arnold (2004) found evidence of oxidative DNA damage in the hippocampus of chronic patients with SCZ [47]. Also, there is evidence of lower level of glutathione peroxidase, which reduces levels of ROS, and dysfunctional mitochondria, especially dysfunctional mitochondrial complex 1, in SCZ [86]. …”

Section: 3 Future Directionsmentioning

confidence: 99%

Β-Amyloid Burden is Not Associated with Cognitive Impairment in Schizophrenia: A Systematic Review

Chung

Nakajima

Plitman

et al. 2016

The American Journal of Geriatric Psychiatry

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Current literature suggests that the pathology of schizophrenia (SCZ) has developmental origins. However, the neurodevelopmental theory of SCZ cannot solely explain several progressive neurodegenerative processes in the illness. There is evidence of accelerated cognitive decline and increased risk of developing dementia in elderly patients with SCZ. Investigating beta-amyloid (Aβ) as a measure of neurodegeneration, we conducted a systematic review focusing on Aβ in patients with SCZ. An OVID literature search using PsychINFO, Medline and Embase database was conducted, looking for studies that compared Aβ levels between patients with SCZ and either elderly controls, patients with AD, or patients with other psychiatric illnesses. Among 14 identified studies, 11 compared Aβ levels between SCZ and elderly controls, seven between SCZ and AD, three between SCZ and other psychiatric illnesses. As a result, no evidence was found suggesting that Aβ levels differ in patients with SCZ from elderly controls or patients with other psychiatric illnesses. All of the seven studies reported lower cortical Aβ levels in patients with SCZ than patients with AD. Furthermore, three out of the four studies, which investigated the relationship between Aβ levels and cognitive impairment in SCZ, observed no association between two factors. The limitations of the included studies are small sample sizes, the inclusion of CSF Aβ or postmortem plaques rather than cortical Aβ assessment in-vivo, and the investigation of different brain regions. In conclusion, Aβ deposition is not associated with cognitive decline in late-life SCZ. Future studies should investigate other neurodegenerative indicators such as oxidative stress and apoptosis dysregulation in SCZ to better understand the pathophysiological mechanisms underlying this illness.

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Oxidative Stress in Schizophrenia

Cited by 205 publications

References 62 publications

DNA Damage in Major Psychiatric Diseases

DNA Damage in Major Psychiatric Diseases

Treatment with d-penicillamine or zinc sulphate affects copper metabolism and improves but not normalizes antioxidant capacity parameters in Wilson disease

Β-Amyloid Burden is Not Associated with Cognitive Impairment in Schizophrenia: A Systematic Review

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