ArticleNeuropsychiatric disease and treatment2017
Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia.
Article in Neuropsychiatric disease and treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Linking Inflammation, Aberrant Glutamate-Dopamine Interaction, and Post-synaptic Changes: Translational Relevance for Schizophrenia and Antipsychotic Treatment: a Systematic Review.Molecular neurobiology · 2022Pooled it
- Mendelian randomization analysis of causal and druggable circulating inflammatory proteins in schizophrenia.Frontiers in psychiatry · 2024Article
- Microglia and cognitive impairment in schizophrenia: translating scientific progress into novel therapeutic interventions.Schizophrenia (Heidelberg, Germany) · 2023Review
- Association betweenAging · 2020Article
- Inflammatory Markers in Anorexia Nervosa: An Exploratory Study.Nutrients · 2018Article
- Haplotypes of TNFDisease markers · 2018Article
- Glial changes in schizophrenia: Genetic and epigenetic approach.Indian journal of psychiatryReview
- Role of TNF-α -308G/A Polymorphism in Bipolar Disorder and its Relationship with Clinical and Demographic Variables.Innovations in clinical neuroscienceArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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
methods
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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