Abstract
There has been increasing evidence that deranged superoxide dismutase (SOD) activities might be a risk factor for schizophrenia and/or tardive dyskinesia (TD). In the present study, we investigated the genetic association between a functional polymorphism (Ala−9Val) in the human manganese (Mn) SOD gene and schizophrenia or TD (192 schizophrenics : 39 with TD and 153 without TD; 141 controls). No significant differences in the allelic or genotypic distribution between schizophrenics and controls were observed. However, we did find a significant difference in genotypic distribution between schizophrenics with and those without TD (p = .03). Moreover, decreased −9Ala (mutant) allele was found among patients with TD (p = .02; odds ratio = 0.29; 95% confidence interval = 0.10–0.83). In conjunction with previous findings of increased free radicals and decreased SOD activities in TD subjects, these results suggest that the−9Ala (high activity) MnSOD allele may play a role in protecting against susceptibility to TD in schizophrenics.
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Acknowledgements
We wish to thank Dr. Akira Etoh, Dr. Yoshitaro Mine, Dr. Yasuhiro Tsutsumi, Dr. Kenji Yamaura, and Dr. Takaharu Hayashida for providing the patient information.
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Hori, H., Ohmori, O., Shinkai, T. et al. Manganese Superoxide Dismutase Gene Polymorphism and Schizophrenia: Relation to Tardive Dyskinesia. Neuropsychopharmacol 23, 170–177 (2000). https://doi.org/10.1016/S0893-133X(99)00156-6
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DOI: https://doi.org/10.1016/S0893-133X(99)00156-6
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