Redox dysregulation as a link between childhood trauma and psychopathological and neurocognitive profile in patients with early psychosis

Alameda, Luis; Fournier, Margot; Khadimallah, Inès; Griffa, Alessandra; Cleusix, Martine; Jenni, Raoul; Ferrari, Carina; Klauser, Paul; Baumann, Philipp S.; Cuénod, Michel; Hagmann, Patric; Conus, Philippe; Q., Kim

doi:10.1073/pnas.1812821115

Cited by 38 publications

(34 citation statements)

References 51 publications

(70 reference statements)

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“…However, it is uncertain whether GPx activity may be decreased in the early stage of this illness because the meta-analysis by Flatow et al did not find any significant difference in its activity between patients with FEP and HCs. Almeda et al demonstrated that, in the early psychosis, patients who had childhood trauma showed smaller hippocampus volume compared with patients who did not have childhood trauma, and that the smaller hippocampus volume was related to higher GPx activity in patients who had childhood trauma (Alameda et al, 2018). They also found higher GPx activity was associated with more severe psychotic symptoms, cognitive impairment, and smaller hippocampus volume in patients with early psychosis who had childhood trauma.…”

Section: Discussionmentioning

confidence: 99%

“…It is also important to identify the subpopulation of patients with SZ who may be able to respond to antioxidative treatment. Previous studies suggested higher GPx activity of patients in the early stage of SZ may reflect higher oxidative stress and link to the efficacy of NAC (Alameda et al, 2018; Conus et al, 2018). These findings warrant further studies to investigate the possible biomarker of the antioxidant treatment response.…”

Section: Summary and Future Directionsmentioning

confidence: 96%

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Glutathione levels and activities of glutathione metabolism enzymes in patients with schizophrenia: A systematic review and meta-analysis

et al. 2019

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Background: Glutathione is among the important antioxidants to prevent oxidative stress. However, the relationships between abnormality in the glutathione system and pathophysiology of schizophrenia remain uncertain due to inconsistent findings on glutathione levels and/or glutathione-related enzyme activities in patients with schizophrenia. Methods: A systematic literature search was conducted using Embase, Medline, PsycINFO, and PubMed. Original studies, in which three metabolite levels (glutathione, glutathione disulfide, and total glutathione (glutathione+glutathione disulfide)) and five enzyme activities (glutathione peroxidase, glutathione reductase, glutamate-cysteine ligase, glutathione synthetase, and glutathione S-transferase) were measured with any techniques in both patients with schizophrenia and healthy controls, were included. Standardized mean differences were calculated to determine the group differences in the glutathione levels with a random-effects model. Results: We identified 41, 9, 15, 38, and seven studies which examined glutathione, glutathione disulfide, total glutathione, glutathione peroxidase, and glutathione reductase, respectively. Patients with schizophrenia had lower levels of both glutathione and total glutathione and decreased activity of glutathione peroxidase compared to controls. Glutathione levels were lower in unmedicated patients with schizophrenia than those in controls while glutathione levels did not differ between patients with first-episode psychosis and controls. Conclusions: Our findings suggested that there may be glutathione deficits and abnormalities in the glutathione redox cycle in patients with schizophrenia. However, given the small number of studies examined the entire glutathione system, further studies are needed to elucidate a better understanding of disrupted glutathione function in schizophrenia, which may pave the way for the development of novel therapeutic strategies in this disorder.

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Section: Discussionmentioning

confidence: 99%

Section: Summary and Future Directionsmentioning

confidence: 96%

Glutathione levels and activities of glutathione metabolism enzymes in patients with schizophrenia: A systematic review and meta-analysis

et al. 2019

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“…Further, the mechanism through which childhood adversity may influence cognition in schizophrenia (e.g., neuroinflammation, neural changes), or any factors that may modulate this mechanism (e.g., gender, genetic or epigenetic processes), remain largely unknown.…”

Section: Recent Developments and Future Directions For Research On Comentioning

confidence: 99%

Nonsocial and social cognition in schizophrenia: current evidence and future directions

2019

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Cognitive impairment in schizophrenia involves a broad array of nonsocial and social cognitive domains. It is a core feature of the illness, and one with substantial implications for treatment and prognosis. Our understanding of the causes, consequences and interventions for cognitive impairment in schizophrenia has grown substantially in recent years. Here we review a range of topics, including: a) the types of nonsocial cognitive, social cognitive, and perceptual deficits in schizophrenia; b) how deficits in schizophrenia are similar or different from those in other disorders; c) cognitive impairments in the prodromal period and over the lifespan in schizophrenia; d) neuroimaging of the neural substrates of nonsocial and social cognition, and e) relationships of nonsocial and social cognition to functional outcome. The paper also reviews the considerable efforts that have been directed to improve cognitive impairments in schizophrenia through novel psychopharmacology, cognitive remediation, social cognitive training, and alternative approaches. In the final section, we consider areas that are emerging and have the potential to provide future insights, including the interface of motivation and cognition, the influence of childhood adversity, metacognition, the role of neuroinflammation, computational modelling, the application of remote digital technology, and novel methods to evaluate brain network organization. The study of cognitive impairment has provided a way to approach, examine and comprehend a wide range of features of schizophrenia, and it may ultimately affect how we define and diagnose this complex disorder.

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“…Furthermore, acute social stress has also been found to increase striatal dopamine release in individuals with a psychotic disorder, and in individuals with CA (Howes et al, 2017). In addition, inflammatory dysfunctions as well as redox dysregulation conditions (Alameda et al, 2018; Steullet et al, 2016) have been found among individuals exposed to CA and among patients with psychosis.…”

Section: Introductionmentioning

confidence: 99%

A systematic review on mediators between adversity and psychosis: potential targets for treatment

et al. 2020

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Various psychological and biological pathways have been proposed as mediators between childhood adversity (CA) and psychosis. A systematic review of the evidence in this domain is needed. Our aim is to systematically review the evidence on psychological and biological mediators between CA and psychosis across the psychosis spectrum. This review followed PRISMA guidelines. Articles published between 1979 and July 2019 were identified through a literature search in OVID (PsychINFO, Medline and Embase) and Cochrane Libraries. The evidence by each analysis and each study is presented by group of mediator categories found. The percentage of total effect mediated was calculated. Forty-eight studies were included, 21 in clinical samples and 27 in the general population (GP) with a total of 82 352 subjects from GP and 3189 from clinical studies. The quality of studies was judged as ‘fair’. Our results showed (i) solid evidence of mediation between CA and psychosis by negative cognitive schemas about the self, the world and others (NS); by dissociation and other post-traumatic stress disorder symptoms; and through an affective pathway in GP but not in subjects with disorder; (iii) lack of studies exploring biological mediators. We found evidence suggesting that various overlapping and not competing pathways involving post-traumatic and mood symptoms, as well as negative cognitions contribute partially to the link between CA and psychosis. Experiences of CA, along with relevant mediators should be routinely assessed in patients with psychosis. Evidence testing efficacy of interventions targeting such mediators through cognitive behavioural approaches and/or pharmacological means is needed in future.

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Redox dysregulation as a link between childhood trauma and psychopathological and neurocognitive profile in patients with early psychosis

Cited by 38 publications

References 51 publications

Glutathione levels and activities of glutathione metabolism enzymes in patients with schizophrenia: A systematic review and meta-analysis

Glutathione levels and activities of glutathione metabolism enzymes in patients with schizophrenia: A systematic review and meta-analysis

Nonsocial and social cognition in schizophrenia: current evidence and future directions

A systematic review on mediators between adversity and psychosis: potential targets for treatment

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