Tardive dyskinesias (TD) are serious side effect symptoms appearing in the course of many years' neuroleptic treatment. On average, TD appear in 20% patients who take neuroleptics chronically. The free radical hypothesis of tardive dyskinesias assumes that they come into existence due to cholinergic neuron damage in the extra-pyramidal system by reactive oxygen species (ROS). Manganese superoxide dismutase (MnSOD) plays a key role in protection against ROS.
Aim: The aim of this study was to evaluate functional gene polymorphism for MnSOD in schizophrenic patients with tardive dyskinesias presence.
Method: 122 paranoid schizophrenia patients were invited to paticipate in the study. TD symptoms were observed in 57 people. The evaluation was performed by applying the PANSS scale, while TD increase was evaluated with the AIMS scale.
Result: Statistical association in allele incidence frequency (p < 0.001) and in a genotype layout was observed between the control group and the schizophrenic group (p < 0.001), and also in a genotype layout between the TD group and the control group (p < 0.001). Allele layout also differentiated the control group and the TD symptoms group (p < 0.05). Relative risk for developing schizophrenia and TD development depends on the genotype in the gene for MnSOD.
Conclusion: In the Polish population there is a statistically substantial association between schizophrenia incidence and the Val-9Val genotype in a gene for MnSOD. Schizophrenic patients having a Val-9Val genotype in the gene for MnSOD have nearly a ten times higher risk for developing TD than schizophrenics not having this genotype. Risk for developing schizophrenia for people having the Val-9Val genotype in the gene for MnSOD is over three times higher than for people lacking this genotype.