Serum tumor necrosis factor-like weak inducer of apoptosis levels are elevated in schizophrenia

Kılıç, Faruk; Işık, Ümit; Usta, Ayşe; Demirdaş, Arif

doi:10.1590/1516-4446-2020-0950

Cited by 5 publications

(4 citation statements)

References 47 publications

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“…13,20 Several types of inflammatory mediators have been found in the serum of schizophrenia patients in higher concentrations, so increased permeability of the BBB leads to CNS inflammation, which may contribute to the disorder. 21,22 In reviewing the literature, no data were found regarding the association between ZO-1 and BBB disruption among patients with schizophrenia. To the best of our knowledge, the present study is the first to investigate serum levels of ZO-1 in schizophrenia patients, and the results of this investigation revealed that schizophrenia patients had significantly higher serum ZO-1 levels than the control group.…”

Section: Discussionmentioning

confidence: 99%

ZO-1 Serum Levels as a Potential Biomarker for Psychotic Disorder

Aydogan Avşar,

Akkuş

2024

Clin Neuropharm

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Objective There are limited studies in the literature on the relationship between intestinal and blood-brain barrier permeability and the etiology of schizophrenia. We hypothesized that the difference in serum ZO-1 levels in patients with schizophrenia may affect the severity of the disease. The aim of this study was to investigate the role of changes in serum ZO-1 concentrations in the etiopathogenesis of patients with schizophrenia. Methods A total of 46 patients, 34 with schizophrenia, 12 with a first psychotic attack, and 37 healthy controls, were included in the study. Symptom severity was determined by applying the Positive and Negative Syndrome Scale and the Clinical Global Impression–Severity Scale. Serum ZO-1 levels were measured from venous blood samples. Results Serum ZO-1 levels were higher in patients with psychotic disorder compared to healthy controls. There was no statistically significant difference between the groups in the first psychotic attack group and the schizophrenia patients. There was a statistically significant positive correlation between serum ZO-1 levels and Positive and Negative Syndrome Scale positive symptom score. Conclusions These findings regarding ZO-1 levels suggest that dysregulation of the blood-brain barrier in psychotic disorder may play a role in the etiology of the disorder.

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Section: Discussionmentioning

confidence: 99%

ZO-1 Serum Levels as a Potential Biomarker for Psychotic Disorder

Aydogan Avşar,

Akkuş

2024

Clin Neuropharm

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“…One of them the tumour necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), is expressed in many tissues including the brain [25]. Kiliç et al [26] was found higher serum TWEAK levels in schizophrenia patients than control groups. Beyazyüz et al [27] showed an increased serum apoptosis level of deficit schizophrenia patients and non-deficit schizophrenia patients compared to healthy controls.…”

Section: Discussionmentioning

confidence: 99%

“…Kiliç et al . [ 26 ] was found higher serum TWEAK levels in schizophrenia patients than control groups. Beyazyüz et al .…”

Section: Discussionmentioning

confidence: 99%

Evaluation Expression of the Caspase-3 and Caspase-9 Apoptotic Genes in Schizophrenia Patients

Dirican

Özcan

Uzunçakmak

et al. 2023

Clin Psychopharmacol Neurosci

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Objective: Apoptosis is programmed cell death that occurs by several pathways. Caspase-3 is induced by active caspase-9 via the intrinsic pathway. The aim of this research was to explore the expression of caspase-3 and caspase-9 in schizophrenia patients and healthy samples. Methods: RNA was isolated from the peripheral blood of 39 schizophrenia patients' and healthy samples. After cDNA synthesis, real time PCR (RT-PCR) was used to analyse caspase-3 and caspase-9 gene expression. The severity of psychopathological symptoms of schizophrenia was evaluated using the Positive and Negative Symptoms Scale for schizophrenia (PANSS) and Clinical Global Impressions (CGI). Results: The expression of caspase-3 and caspase-9 genes was higher in schizophrenia patients than in healthy samples (p = 0.012, p = 0.002, respectively). The increase in caspase-3 gene expression was significant with being male, smoking and with a duration of less than 6 years (p = 0.047, p = 0.049, p = 0.034, respectively). On the other hand, the increase in caspase-9 gene expression was significant in patients who is smoke, have children, and are under 33 years old (p = 0.040, p = 0.043, p = 0.045, respectively). A significant positive correlation was detected between the caspase-3 and caspase-9 gene expression (r = 0.3218, p = 0.049). Conclusion:Our findings indicate that caspase-3 and caspase-9 gene expression may activate cell death mechanisms by intrinsic apoptotic genes. Furthermore, caspase-3 and caspase-9 may play essential roles in different ways in schizophrenia. Hence there is a need to further study the apoptotic mechanism with expanded patient populations.

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“…Additionally, the relationship between TWEAK and TJ protein dysregulation reaches to further neurological diseases where the BBB’s architecture is disturbed, for instance in schizophrenia [ 26 ]. Two recent studies found that TWEAK serum levels are significantly elevated in schizophrenic patients [ 27 ], and claudin-5 levels are significantly lowered [ 28 ]. Thus, restoring claudin-5 function via TWEAK inhibition could serve as a potential therapeutic solution for multiple neurodegenerative diseases, and MS in particular.…”

Section: Discussionmentioning

confidence: 99%

TWEAK and TNFα, Both TNF Ligand Family Members and Multiple Sclerosis-Related Cytokines, Induce Distinct Gene Response in Human Brain Microvascular Endothelial Cells

Stephan

Roger

Aghzadi

et al. 2022

Genes

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Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the TNF ligand family involved in various diseases including brain inflammatory pathologies such as multiple sclerosis. It has been demonstrated that TWEAK can induce cerebrovascular permeability in an in vitro model of the blood–brain barrier. The molecular mechanisms playing a role in TWEAK versus TNFα signaling on cerebral microvascular endothelial cells are not well defined. Therefore, we aimed to identify gene expression changes in cultures of human brain microvascular endothelial cells (hCMEC/D3) to address changes initiated by TWEAK exposure. Taken together, our studies highlighted that gene involved in leukocyte extravasation, notably claudin-5, were differentially modulated by TWEAK and TNFα. We identified differential gene expression of hCMEC/D3 cells at three timepoints following TWEAK versus TNFα stimulation and also found distinct modulations of several canonical pathways including the actin cytoskeleton, vascular endothelial growth factor (VEGF), Rho family GTPases, and phosphatase and tensin homolog (PTEN) pathways. To our knowledge, this is the first study to interrogate and compare the effects of TWEAK versus TNFα on gene expression in brain microvascular endothelial cells.

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Serum tumor necrosis factor-like weak inducer of apoptosis levels are elevated in schizophrenia

Cited by 5 publications

References 47 publications

ZO-1 Serum Levels as a Potential Biomarker for Psychotic Disorder

ZO-1 Serum Levels as a Potential Biomarker for Psychotic Disorder

Evaluation Expression of the Caspase-3 and Caspase-9 Apoptotic Genes in Schizophrenia Patients

TWEAK and TNFα, Both TNF Ligand Family Members and Multiple Sclerosis-Related Cytokines, Induce Distinct Gene Response in Human Brain Microvascular Endothelial Cells

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