The forkhead-box P2 (FOXP2) gene polymorphism has been reported to be involved in the susceptibility to schizophrenia; however, few studies have investigated the association between FOXP2 gene polymorphism and clinical symptoms in schizophrenia. This study investigated whether the FOXP2 gene was associated with the development and symptoms of schizophrenia in relatively genetically homogeneous Chinese population. The FOXP2 rs10447760 polymorphism was genotyped in 1069 schizophrenia inpatients and 410 healthy controls using a case-control design. The patients' psychopathology was assessed by the Positive and Negative Syndrome Scale (PANSS). We found no significant differences in the genotype and allele distributions between the patient and control groups. Interestingly, we found significant differences in PANSS total, positive symptom, and general psychopathology scores between genotypic subgroups in patients, with the higher score in patients with CC genotype than those with CT genotype (all p < 0.05). After adjusting demographic and clinical variables, the difference still remained significant for the PANSS positive symptom score and general psychopathology (both p < 0.05). Our findings suggest that the FOXP2 rs10447760 polymorphism may not contribute to the development of schizophrenia, but may contribute to the clinical symptoms of schizophrenia among Han Chinese.
Recent compelling research has demonstrated a pathophysiologic role for proinflammatory cytokines of microglial origin in decreasing neurocognitive function. Psychiatric diseases are already known to have reduced cognitive function and are also associated with increased inflammation. To elaborate on these data, our study aims to investigate how a particular polymorphism of the tumor necrosis factor gene, TNF-α -1031T/C, affects neurocognitive performance in patients with schizophrenia. We recruited 905 patients with schizophrenia and 571 healthy control subjects. We employed the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) to test for neurocognitive function and the positive and negative syndrome scale to evaluate schizophrenia severity. The -1031T/C polymorphism was genotyped in both healthy controls and schizophrenic patients. Our results demonstrate that patients with the C allele (either T/C or C/C) possessed increased immediate memory index, visuospatial/constructional index, and RBANS total scores as compared to patients without it (p < .05). In healthy controls, there was no significant difference across genotypes (p > .05). Our findings demonstrate that the TNF-α -1031T/C polymorphism may not play a role in the susceptibility of schizophrenia itself, but may be involved in the cognitive deficits of schizophrenia. This suggests an important role for cytokine signaling in mediating the severity of cognitive dysfunction in schizophrenia.
Objective: Evidence has shown the importance of tumor necrosis factor alpha (TNF-alpha) in the pathophysiological feature in schizophrenia patients. This study aims to determine the impact of a single-nucleotide polymorphism (SNP) in the TNF-alpha gene promoter on the susceptibility, onset age, and cognitive function of schizophrenia. Method: The SNP −1031T>C in the TNF-alpha gene was genotyped in 905 patients and 571 healthy controls. The Positive and Negative Syndrome Scale (PANSS) was used to assess the schizophrenia symptoms and the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) for cognitive function. Results: There was no significant difference in allele or genotype distribution of the SNP −1031T>C between patients and controls (p = .85, p = .98). This polymorphism had no significant genotypic effect on the symptomatology assessed by the PANSS. Interestingly, this polymorphism was significantly correlated with onset age in schizophrenia patients (p = .004). We found an earlier onset age in patients with the TT genotype compared to those with the CT and CC genotypes (both p < .05). Moreover, there were significant genotypic effects on the immediate memory index, visuospatial/constructional index, and RBANS total score (all p < 0.05) in the patient group. Conclusions: Our results suggest that the SNP −1031T>C of the TNF-alpha gene may not be associated with susceptibility to schizophrenia but possibly acts as a modulator for its onset age as well as for cognitive deficits.
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