TNF-related weak inducer of apoptosis (TWEAK) levels in schizophrenia

Yaylacı, Elif Tatlıdil; Yüksel, Rabia Nazik; Ünal, Kübranur; Altunsoy, Neslihan; Cingi, Merve; Sahiner, Safak Yalcin; Aydemir, Makbule Çiğdem; Göka, Erol

doi:10.1016/j.psychres.2015.08.006

Cited by 6 publications

(3 citation statements)

References 45 publications

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“…Only one study has investigated TWEAK levels in schizophrenia. 27 Unlike in our study, Tatlidil Yaylaci et al 27 found no significant differences in serum TWEAK levels in patients with schizophrenia compared to healthy controls, although they found that TWEAK levels in male patients were significantly lower than in male controls. It is stated in the literature that some confounding factors, such as age, smoking, BMI, and gender, may affect the inflammatory system.…”

Section: Discussioncontrasting

confidence: 92%

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

Kılıç

Işık

Usta

et al. 2021

Braz. J. Psychiatry

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The purpose of this study was to assess serum Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) concentrations to determine whether changes in patients with schizophrenia could have etiopathogenetic importance. Since very little research has addressed the connection between the inflammatory marker TWEAK and schizophrenia, we wanted to examine alterations of TWEAK and investigate the possible correlation between clinical symptomatology and serum concentrations. Methods: A total of 45 schizophrenia patients and 40 healthy controls were included in this study. The Positive Symptom Assessment scale and the Negative Symptom Assessment scale were administered to determine symptom severity. Venous blood samples were collected and serum TWEAK levels were measured. Results: Serum TWEAK levels were significantly higher in the schizophrenia group than the control group, independently of potential confounders, including sex, age, body mass index and smoking status. Conclusion: The results indicate that TWEAK is elevated in schizophrenia patients, which could deepen our understanding of the role of inflammation in the pathogenesis of schizophrenia.

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Section: Discussioncontrasting

confidence: 92%

“… 23 - 26 To the best of our knowledge, only one study has investigated TWEAK levels in schizophrenia. 27 Given the importance of neuroinflammation changes in schizophrenia, biomarkers of persistent inflammation are needed, especially in view of therapeutics.…”

Section: Introductionmentioning

confidence: 99%

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

Kılıç

Işık

Usta

et al. 2021

Braz. J. Psychiatry

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“…Recently, TWEAK plasma levels of patients suffering from schizophrenia were compared with controls. Although no difference was shown globally, TWEAK levels in male patients were significantly lower than in male controls, suggesting TWEAK involvement in subgroups of schizophrenia patients ( 62 ). In bipolar disorder, conflicting results were observed, perhaps due to the heterogeneity in patients’ groups: Cingi et al measured lower TWEAK plasma levels compared to healthy controls ( 63 ), while Barbosa et al described increased concentrations, regardless of the mood ( 64 ).…”

Section: Tweak Contribution To Parkinson’s Disease and Psychiatric DImentioning

confidence: 79%

Regulation of Neuroinflammation: What Role for the Tumor Necrosis Factor-Like Weak Inducer of Apoptosis/Fn14 Pathway?

Boulaméry

Desplat‐Jégo

2017

Front. Immunol.

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Observed in many central nervous system diseases, neuroinflammation (NI) proceeds from peripheral immune cell infiltration into the parenchyma, from cytokine secretion and from oxidative stress. Astrocytes and microglia also get activated and proliferate. NI manifestations and consequences depend on its context and on the acute or chronic aspect of the disease. The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/Fn14 pathway has been involved in chronic human inflammatory pathologies such as neurodegenerative, autoimmune, or malignant diseases. New data now describe its regulatory effects in tissues or fluids from patients with neurological diseases. In this mini-review, we aim to highlight the role of TWEAK/Fn14 in modulating NI in multiple sclerosis, neuropsychiatric systemic lupus erythematosus, stroke, or glioma. TWEAK/Fn14 can modulate NI by activating canonical and non-canonical nuclear factor-κB pathways but also by stimulating mitogen-activated protein kinase signaling. These downstream activations are associated with (i) inflammatory cytokine, chemokine and adhesion molecule expression or release, involved in NI propagation, (ii) matrix-metalloproteinase 9 secretion, implicated in blood–brain barrier disruption and tissue remodeling, (iii) astrogliosis and microgliosis, and (iv) migration of tumor cells in glioma. In addition, we report several animal and human studies pointing to TWEAK as an attractive therapeutic target.

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Methamphetamine modulates the production of interleukin-6 and tumor necrosis factor-alpha via the cAMP/PKA/CREB signaling pathway in lipopolysaccharide-activated microglia

Wang

Chen

Wang

et al. 2018

International Immunopharmacology

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TNF-related weak inducer of apoptosis (TWEAK) levels in schizophrenia

Cited by 6 publications

References 45 publications

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

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

Regulation of Neuroinflammation: What Role for the Tumor Necrosis Factor-Like Weak Inducer of Apoptosis/Fn14 Pathway?

Methamphetamine modulates the production of interleukin-6 and tumor necrosis factor-alpha via the cAMP/PKA/CREB signaling pathway in lipopolysaccharide-activated microglia

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