Objective: Previous studies have indicated that the immune may be involved in the pathogenesis of tardive dyskinesia (TD). Some genetic polymorphisms in the human leukocyte antigen (HLA) I and II regions have been associated with TD, and the tumor necrosis factor-α (TNF-α) gene is located in the HLA III region. TNF-α levels in the striatum significantly increased in haloperidol-induced TD in rats. The TNF-α gene -308A/G single nucleotide polymorphism (SNP) has been shown to directly influence TNF-α expression. The genetic association between the TNF-α gene -308A/G SNP and TD is unclear. The present study investigated whether this variation is associated with clinical phenotypes and TD in schizophrenia in a genetically homogeneous northern Chinese Han population.
Methods: We genotyped the TNF-α gene -308A/G SNP in patients with schizophrenia with TD (n=350) and without TD (n=410). The Abnormal Involuntary Movement Scale (AIMS) and Positive and Negative Syndrome Scale (PANSS) were used to assess the severity of TD and psychopathology of schizophrenia, respectively.
Results: The allele and genotype frequencies did not significantly differ between patients with schizophrenia with and without TD (p>0.05). No significant difference was found in the total AIMS score between the genotypes (p>0.05). However, the PANSS negative symptom subscore was associated with risk for TD (p=0.004), and a significant difference was found in total AIMS score between the genotypes in TD patients (p=0.013).
Conclusion: The TNF-α gene -308A/G polymorphism does not appear to play a major role in the susceptibility to TD in patients with schizophrenia in a northern Chinese Han population. However this polymorphism may play a role in the TD severity.
Copyright Â© 2011 Elsevier Inc. All rights reserved.