The relationship between psychopathology and cognitive functions with cytokines in clinically stable patients with schizophrenia

Abstract

OBJECTIVES: Inflammation and the cytokine hypotheses have been proposed for schizophrenia. Several proinflammatory and anti-inflammatory cytokines have been studied in drug-naive, first-episode, and/or chronic schizophrenia patients. However, there were limited data on clinical stable outpatients reflecting daily routine. The aim of this study was to compare the serum levels of cytokines, including transforming growth factor-beta (TGF-β), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α), between clinically stable patients with schizophrenia and healthy controls, as well as to examine the relationship between these inflammation parameters and clinical variables (positive and negative symptom severity and cognitive functions). METHODS: Thirty clinically stable outpatients with schizophrenia and 30 healthy controls with similar sex and age were included in this study. Serum IL-6, TGF-β, and TNF-α levels were assessed by enzyme-linked immunosorbent assay (ELISA) and immunoenzyme microplate measurement, respectively. Illness severity was evaluated using the Positive and Negative Syndrome Scale (PANSS), and the cognitive functions of the participants were assessed using a broad neuropsychological test battery. RESULTS: The serum levels of IL-6 and TGF-β were significantly higher in patients with schizophrenia compared to healthy controls (p = .048, p = .012). There was no significant difference between groups in terms of TNF-α levels (p = .726). Global impairment of cognitive functions was observed in the patient group compared to healthy controls, and PANSS scores and cognitive functions showed no correlation with cytokine levels (IL-6, TNF-α, and TGF-β). CONCLUSIONS: The present study demonstrated an increased inflammatory response in clinically stable patients with schizophrenia compared to healthy controls. However, symptom severity and cognitive functions showed no correlation with cytokine levels. Further research studies are needed to clarify the effects of cytokine levels on schizophrenia symptomatology and etiopathogenesis.

Knowledge Graphs for Indication Expansion: An Explainable Target-Disease Prediction Method

“…The predicted TGFB1-Mental Disorders link, which later were published in López-González et al (2019 ), supports the theory that dysfunction of the immune system plays an important role in the etiology of mental illnesses, such as schizophrenia and depression ( Frydecka et al, 2013 ; Bialek et al, 2020 ). In fact, significantly higher serum levels of the IL-6 and TGFB1 cytokines have been reported in patients with schizophrenia compared to healthy controls ( Ergün et al, 2017 ) and mutations in TGFB1 have been associated with the susceptibility and treatment response of schizophrenia ( Frydecka et al, 2013 ) and major depressive disorder ( Bialek et al, 2020 ).…”

Cytokine Level and Symptoms of Schizophrenia

“…Table 2 showed that in the schizophrenia group, statistically, there was no significant correlation between TNF-alpha level and PANSS score (p = 0.594), the correlation was very weak, but it had a positive correlation means that the higher TNF-alpha level was, the higher PANSS score would be. Ergün et al also reported the lack of correlation between TNF-alpha and PANSS score, [13], with a negative correlation direction. Kubistova et al [14], Ajami et al [15], and Luo et al [16] reported similar results, who found that there was no TNF-alpha correlation with PANSS score on PwS.…”

Role of Tumor Necrosis Factor-Alpha in Schizophrenia and Cognitive Impairment

“…In patients with schizophrenia, elevated cytokine levels such as TNF-α, transform beta growth factor, IL-6, IL-1β receptor, IL-1 blocker, IL-2 receptor, and IL-12 receptor have been identified; however, numerous studies have also found some controversial results. These variations relate to the determination of exclusion criteria, nature of the study, sample size, patient clinical status, metabolic and/or inflammatory disorder comorbidity, body mass index (BMI) potential effects, and smoking status may all cause differences in this variation [10].…”