Reduced serum TNF alpha level in chronic schizophrenia patients with or without tardive dyskinesia

Tian, Li; Tan, Yunlong; Chen, Dachun; Lv, Menghan; Tan, Shuping; Soares, Jair C.; Zhang, Xiang Yang

doi:10.1016/j.pnpbp.2014.06.012

Cited by 29 publications

(17 citation statements)

References 61 publications

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“…Alterations in the serum TNF-α level of chronic schizophrenia patients have been reported previously,56–58 implicating the role of TNF-α and TNF-α-related signaling pathways in the pathophysiology of schizophrenia. The roles of TNF-α in controlling neuronal excitability and metabolisms of glutamate, dopamine, and serotonin neurotransmitters have made it an outstanding candidate for etiology and pathophysiology of schizophrenia 59. It has been suggested that TNF-α may be a trait marker of schizophrenia and may have an important role in the psychopathology of schizophrenia 60,61.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

Kadasah¹,

Arfin²,

Rizvi³

et al. 2017

NDT

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BackgroundSchizophrenia is one of the most common devastating psychiatric disorders that negatively affects the quality of life and psychosocial functions. Its etiology involves the interplay of complex polygenic influences and environmental risk factors. Inflammatory markers are well-known etiological factors for psychiatric disorders, including schizophrenia.ObjectiveThe aim of this study was to investigate the association of proinflammatory cytokine genes, tumor necrosis factor (TNF)-α (−308G/A) and TNF-β (+252A/G) polymorphisms with schizophrenia susceptibility.Subjects and methodsTNF-α and TNF-β genes were amplified using amplification refractory mutation system primers in 180 schizophrenia patients and 200 healthy matched controls recruited from the Psychiatry Clinic of Prince Sultan Military Medical City, Riyadh. The frequencies of alleles and genotypes of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms in patients were compared with those in controls.ResultsThe frequencies of TNF-α (−308) allele A and genotype GA were significantly higher, while those of allele G and genotype GG were lower in schizophrenia patients as compared to controls, indicating that genotype GA and allele A of TNF-α (−308G/A) may increase susceptibility to schizophrenia, while genotype GG and allele G may reduce it. On the other hand, the distribution of alleles and genotypes of TNF-β (+252A/G) polymorphism does not differ significantly in patients from controls; however, the frequency of genotype GG of TNF-β (+252A/G) was significantly higher in male patients than in female patients. The distribution of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms was almost similar in schizophrenia patients with negative or positive symptoms.ConclusionTNF-α (−308G/A) and TNF-β (+252G/A) polymorphisms may increase the susceptibility to schizophrenia in Saudi patients and could be a potential risk factor for its etiopathogenesis. However, further studies are warranted involving a larger sample size to strengthen our findings.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

Kadasah¹,

Arfin²,

Rizvi³

et al. 2017

NDT

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“…TNF-α plays a key role in mediating the complex events involved in inflammation and immunity. The roles of TNF-α in controlling neuronal excitability and metabolisms of glutamate, dopamine, and serotonin neurotransmitters make it an outstanding candidate for etiology and pathophysiology of schizophrenia (Tian et al, 2014). Alterations in serum TNF-α level in chronic schizophrenia patients have been reported previously, but with inconsistent results, being no different (Pedrini et al, 2012; Kunz et al, 2011), elevated (Lin et al, 1998; Naudin et al, 1997; Beumer et al, 2012; García-Miss et al, 2010; Luo et al, 2014) or reduced (Francesconi et al, 2011; Lv et al, 2014; Potvin et al, 2008), as compared with healthy control subjects.…”

Section: Discussionmentioning

confidence: 99%

Relationship of serum levels of TNF-α, IL-6 and IL-18 and schizophrenia-like symptoms in chronic ketamine abusers

Fan

Luo

Zhang

et al. 2015

Schizophrenia Research

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Objective Exposing to NMDAR receptor antagonists, such as ketamine, produces schizophrenia-like symptoms in humans and deteriorates symptoms in schizophrenia patients. Meanwhile, schizophrenia is associated with alterations of cytokines in the immune system. This study aims to examine the serum TNF-α, IL-6 and IL-18 levels in chronic human ketamine users as compared to healthy subjects. The correlations between the serum cytokines levels with the demographic, ketamine use characteristics and psychiatric symptoms were also assessed. Methods 155 subjects who fulfilled the criteria of ketamine dependence and 80 healthy control subjects were recruited. Serum TNF-α, IL-6 and IL-18 levels were measured using an enzyme-linked immunosorbent assay (ELISA). The psychiatric symptoms of the ketamine abusers were assessed using the Positive and Negative Syndrome Scale (PANSS). Results Serum IL-6 and IL-18 levels were significantly higher, while serum TNF-α level was significantly lower among ketamine users than among healthy controls (p < 0.05). Serum TNF-α levels showed a significant negative association with PANSS total score (r = −0.210, p < 0.01) and negative subscore (r = −0.300, p < 0.01). No significant association was found between PANSS score and serum levels of IL-6 and IL-18. Conclusions Serum levels of TNF-α, IL-6 and IL-18 were altered in chronic ketamine abusers which may play a role in schizophrenia-like symptoms in chronic ketamine abusers.

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“…TNF-α has important roles in neurogenesis, neuronal cell death, and innate and adaptive immune response (19). Studies on TNF-α vary from higher levels (15, 20–29), no difference (30–40), and lower levels in schizophrenia (41–45). IL-6 has pro-inflammatory and, under certain conditions, anti-inflammatory effects (46), and was elevated in nearly two-thirds of the published reports (15, 22, 24, 28, 29, 35–39, 44, 47–62), no different in a third (20, 21, 23, 26, 30–32, 34, 45, 63–67), and lower in schizophrenia in one study (68).…”

Section: Objectivementioning

confidence: 99%

Inflammation in Schizophrenia: Cytokine Levels and Their Relationships to Demographic and Clinical Variables

Lee

Hong

Martin

et al. 2017

The American Journal of Geriatric Psychiatry

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Objective Inflammation may play a role in the accelerated physical aging reported in schizophrenia though biomarker findings and associations with demographic and clinical factors are inconsistent. Design Cross-sectional, case-control design Setting Community-dwelling participants tested in an academic laboratory. Participants 95 outpatients with schizophrenia (mean age ± SD: 48.1 ± 10.2 yrs) and 95 demographically-comparable healthy comparison subjects (HCs) (mean age ± SD: 48.1 ± 12.1 yrs) Measurements Sociodemographic and clinical data were collected, and plasma levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ) were assayed. We compared cytokine levels, examined demographic and clinical associations. and adjusted for relevant variables with linear models. Results Individuals with schizophrenia had higher levels of TNF-α and IL-6, but not IFN-γ, than HCs. Age was not related to cytokine levels, and age relationships did not differ between diagnostic groups. Women had higher levels of IL-6. TNF-α and IL-6 levels were significantly correlated with depressive symptoms, and adjustment for depression reduced the group effect for both. Within the HCs, TNF-α levels were associated with physical comorbidity and body mass index (BMI). IL-6 levels were significantly correlated with BMI, and within schizophrenia patients, with worse mental and physical well-being. Accounting for physical morbidity and mental well-being reduced group differences in TNF-α and IL-6 levels, respectively. Worse positive symptoms were associated with higher IL-6 levels. Conclusions Higher TNF-α and IL-6 levels in schizophrenia patients were associated with depression, physical comorbidity, and mental well-being. Further longitudinal studies are warranted to assess inflammation as a potential treatment target for a subgroup of schizophrenia.

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Reduced serum TNF alpha level in chronic schizophrenia patients with or without tardive dyskinesia

Cited by 29 publications

References 61 publications

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

Relationship of serum levels of TNF-α, IL-6 and IL-18 and schizophrenia-like symptoms in chronic ketamine abusers

Inflammation in Schizophrenia: Cytokine Levels and Their Relationships to Demographic and Clinical Variables

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Reduced serum TNF alpha level in chronic schizophrenia patients with or without tardive dyskinesia

Cited by 29 publications

References 61 publications

Tumor necrosis factor-&alpha; and -&beta; genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

Tumor necrosis factor-&alpha; and -&beta; genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

Relationship of serum levels of TNF-α, IL-6 and IL-18 and schizophrenia-like symptoms in chronic ketamine abusers

Inflammation in Schizophrenia: Cytokine Levels and Their Relationships to Demographic and Clinical Variables

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Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia