Kadasah Saeed, Arfin Misbahul, Rizvi Sadaf, Al-Asmari Mohammed, Al-Asmari Abdulrahman
Department of Psychiatry.
Division of Molecular Biology & Genetics, Scientific Research Center, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.
Neuropsychiatr Dis Treat. 2017 Apr 12;13:1081-1088. doi: 10.2147/NDT.S131144. eCollection 2017.
Schizophrenia 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.
The 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.
and 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.
The 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.
TNF-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.
精神分裂症是最常见的具有破坏性的精神障碍之一，会对生活质量和心理社会功能产生负面影响。其病因涉及复杂的多基因影响与环境风险因素之间的相互作用。炎症标志物是包括精神分裂症在内的精神障碍的知名病因。
本研究旨在探讨促炎细胞因子基因、肿瘤坏死因子（TNF）-α（-308G/A）和TNF-β（+252A/G）多态性与精神分裂症易感性之间的关联。
从利雅得苏丹王子军事医疗城精神病诊所招募了180例精神分裂症患者和200例健康对照，使用扩增阻滞突变系统引物扩增 和 基因。将患者中TNF-α（-308G/A）和TNF-β（+252A/G）多态性的等位基因和基因型频率与对照进行比较。
与对照相比，精神分裂症患者中TNF-α（-308）等位基因A和基因型GA的频率显著更高，而等位基因G和基因型GG的频率更低，这表明TNF-α（-308G/A）的基因型GA和等位基因A可能增加精神分裂症的易感性，而基因型GG和等位基因G可能降低易感性。另一方面，TNF-β（+252A/G）多态性的等位基因和基因型在患者与对照中的分布无显著差异；然而，男性患者中TNF-β（+252A/G）基因型GG的频率显著高于女性患者。有阴性或阳性症状的精神分裂症患者中TNF-α（-308G/A）和TNF-β（+252A/G）多态性的分布几乎相似。
TNF-α（-308G/A）和TNF-β（+252G/A）多态性可能增加沙特患者患精神分裂症的易感性，并且可能是其发病机制的潜在风险因素。然而，需要进一步开展涉及更大样本量的研究以强化我们的发现。
