Tardive Dyskinesia Development, Superoxide Dismutase Levels, and Relevant Genetic Polymorphisms

Uludag, Kadir; Wang, Dong Mei; Zhang, Xiang Yang

doi:https://doi.org/10.1155/2022/5748924

Oxidative Medicine and Cellular Longevity

On this page

Abstract Introduction Methods Results Discussion Conclusion Limitations Abbreviations Additional Points Conflicts of Interest Acknowledgments References Copyright Related Articles

Review Article | Open Access

Volume 2022 | Article ID 5748924 | https://doi.org/10.1155/2022/5748924

Tardive Dyskinesia Development, Superoxide Dismutase Levels, and Relevant Genetic Polymorphisms

Kadir Uludag,¹Dong Mei Wang,¹and Xiang Yang Zhang¹

Academic Editor: Vladimir Jakovljevic

Received08 Aug 2022

Revised22 Sept 2022

Accepted06 Oct 2022

Published28 Oct 2022

Abstract

Tardive dyskinesia (TD) is a prevalent movement disorder that significantly impacts patients with schizophrenia (SCZ) due to extended exposure to antipsychotics (AP). Several genetic polymorphisms, including superoxide dismutase (SOD) and DRD3 9ser, have been suggested as explanations why some patients suffer from TD. Methods. A PubMed search was used to search relevant articles using the following keywords: “Tardive Dyskinesia and Superoxide Dismutase”. Fifty-eight articles were retrieved. Among them, 16 were included in this review. Results. Overall, 58 studies were retrieved from PubMed. Most studies investigated the association between TD and the SOD-related polymorphisms. In addition, previous studies reported an association between TD occurrence and other genetic polymorphisms. Conclusion. This study found that the risk of TD is associated with altered SOD levels and several genetic polymorphisms, including VAL 66 Met and DRD3 9ser.

1. Introduction

Tardive dyskinesia (TD) is a movement disorder that occurs due to an excessive exposure to antipsychotics (AP), an essential problem in schizophrenia (SCZ) patients since they need to use APs for an extended period [1]. However, it is unclear why some patients develop TD, while some do not, and therefore, genetic studies have been done to try to account for the susceptibility to TD [2]. The superoxide dismutase (SOD) polymorphism is one of the candidates reported to be related to TD occurrence. SODs are universal enzymes [3] that have an essential role in inflammatory diseases [4] and oxidative stress (OS) [5]. Therefore, due to their relation to these diseases, they are associated with cognitive functions such as memory and attention.

Many previous studies have found an association between serum SOD levels and TD occurrence [6, 7]. Additionally, SCZ patients with TD have lower copper-zinc couple SOD (CuZnSOD) activity than non-TD patients [8]. Similarly, a different study found a decrease in erythrocyte SOD activity in the TD group than the non-TD group [9].

Recently, genetic studies concerning TD susceptibility have gained importance, and the combination of the MnSOD-9val and DRD3 9ser alleles has been associated with TD (Z. J. [10]). Furthermore, a study found that the excess of the -697 variant in the promoter regulation of the HTR2C gene may be a risk factor for TD [10, 11]. However, a different study did not support the previous findings and reported that the MnSOD gene Ala-9Val polymorphism did not have a role in TD risk [12].

It is crucial to consider that the previous studies may have adopted different methods to investigate the association between SOD and TD, and taken together, systematically exploring the association between TD and SOD-related parameters is vital. Furthermore, we have investigated the association between TD and SOD-related parameters according to inflammation and OS concerning cognitive deficits.

2. Methods

A PubMed search was used to find articles relevant to tardive dyskinesia (TD) and superoxide dismutase (SOD) using the keywords “tardive dyskinesia and superoxide dismutase”. Overall, 58 articles were found. Animal studies were excluded from this study, as well as non-English articles, articles prior to 1997, and articles not relevant to this research question. All the included studies were written in English and published between 1997 and 10 June 2022 (total of 16 studies were included).

SOD activity is not simply observed directly due to the rapid substrate disappearance at physiological pH [13]. SOD levels can be measured in several ways, including in serum and erythrocytes. For most of the studies mentioned in this review, determination of plasma total SOD activities was executed using an assay involving spectrophotometric determination as in previous study [14]. In addition, genotyping was performed by polymerase chain reaction (PCR). For some studies, the genotypes were combined by their functional significance to investigate the interaction between polymorphisms.

There are no well-established and comprehensive methods for measuring OS in SCZ patients [15]. Overall, the techniques for measuring OS include reactive oxygen species (ROS) fingerprinting and ROS in body fluids [16]. In addition, OS can be investigated in the peripheral and central nervous systems. Moreover, regional variations in OS in human skin can be observed [17]. However, it is essential to note that antioxidant capacity markers are suggested to be associated with oxidative damage markers, although they are insufficient [18]. Several methods have been used to investigate oxidative base modifications, including gas and liquid chromatography [19]. Additionally, developing technology has helped to determine the location of oxidation-related DNA damage [19].

3. Results

A total of 16 articles were retrieved related to tardive dyskinesia (TD) and superoxide dismutase (SOD) and included in this study (Table 1). In addition, a few articles were also related to cognitive skills and TD.

3.1. Results of Studies Related to Superoxide Dismutase-Related Polymorphisms

The included studies investigated the association between TD and Ala-9Val, DRD3 9ser, NQO1 Pro187Ser, and HTR2C polymorphisms. Furthermore, the studies investigated the combination of genes, including the combination of the MnSOD -9val and CAT-262C>T, and DRD3 9ser alleles were associated with TD [10, 11]. The combined genotypes of T/T in NQO1 Pro187Ser and Val/Val in MnSOD Ala-9Val polymorphisms were associated with a higher TD risk [20]. In addition, the excess of the -697 variant in the promoter regulation of the HTR2C gene may be a risk factor for TD [10, 11]. Moreover, no critical roles of SOD2Val16Ala, CAT-262C>T, and GPX1Pro200Leu polymorphisms in TD occurrence were found [21].

3.2. Results of Studies Related to Serum Superoxide Dismutase Levels

Several studies investigated the relationship between SOD serum levels and TD occurrence.

One study showed lower CuZnSOD activity in patients with TD than those without TD [6, 7]. Furthermore, SCZ patients with TD had lower CuZnSOD activity than patients without TD [8].

Another study showed that MnSOD activity was lower in patients with TD than in non-TD patients [22]. In addition, a different study showed a decrease in erythrocyte SOD activity in the TD group compared with the non-TD group [9].

4. Discussion

This study found that superoxide dismutase (SOD) is vital in understanding the risk of TD occurrence and may be used as a biomarker to predict TD occurrence. Moreover, most of the studies related to genetics were focused on the SOD-related polymorphisms.

Despite the common literature, the papers were difficult to compare due to the differences in study samples, including age, study design, comorbid disorders, and hospitalization status; the aim of the studies; and the methodologies.

SOD regulates OS, inflammation, and oxidation [23]. Some environmental factors may also be associated with MnSOD, such as exercise [24]. In addition, some studies mentioned the link between SOD-related parameters and cognitive skills.

TD-related theories focused on postsynaptic D2 receptor supersensitivity and dopamine hyperactivity [25] while D2 receptor hypersensitivity and degenerative changes in the neurons due to exposure to oxidative stress (OS) can lead to impacts on the synaptic plasticity of glutamatergic synapses, leading to an imbalance between pathways of basal ganglia and creating aberrant output to the sensorimotor cortex [26, 27]. Therefore, OS-related parameters may be used to understand TD mechanisms.

4.1. The Relationship between Superoxide Dismutase (SOD) and Oxidative Stress

Superoxide is a prevalent ROS produced by the mitochondria [28]. SODs are essential in treating OS-related diseases [29], and elevated SOD was related to lower mortality in older females [30]. A balance in ROS is essential, and SOD, a normal metabolite in standard amounts, facilitates critical roles [5]. The structure and location of SODs are vital for a healthy balance of superoxides [31]. Therefore, therapeutics targeting oxidation and superoxides should be investigated for treating neurodegeneration [32].

4.2. The Relationship between Superoxide Dismutase (SOD) and Cognitive Skills

Previous studies have investigated the association between SOD and specific cognitive functions and have found that extracellular SOD played a vital role in various cognitive functions [33]. Another study demonstrated the role of reactive oxygen species (ROS) in learning deficit (R. [34]).

Studies with animal models that overexpressed superoxide scavengers demonstrated that some neuronal processes are changed during diminished superoxide-related signaling [35]. Furthermore, a different study suggested that participants with late-life SCZ had disturbances in their antioxidant system, which was related to cognitive problems [36]. Therefore, an antioxidant with mitochondrial activity may improve cognitive impairments [37]. One study investigated changes in SOD levels after antioxidant kaempferol use and demonstrated increased SOD and diminished memory problems in rats [38]. Moreover, it has also been found that low SOD was related to an increased risk of poststroke cognitive deficiency (M.-S. [39]).

Taken together, SOD may play an essential role in cognitive skills, and antioxidants may relieve TD symptoms.

4.3. Antioxidant Treatment on Relieving Tardive Dyskinesia Symptoms

Some antioxidants, including Ginkgo biloba, vitamin E, omega 3, piracetam, and curcumin, could reduce the severity of TD symptoms ([40]; X. Y. [41]). Elsewhere, it has been found that resveratrol enhanced the expression of antioxidant enzymes such as heme oxygenase 1 and SOD, which are responsible for redox balance [42]. Consequently, antioxidants have been commonly suggested to possibly alleviate the severity of TD symptoms through oxidative mechanisms.

5. Conclusion

In conclusion, SOD levels and several SOD polymorphisms (e.g., MnSOD -9val and DRD3 9ser) are vital in understanding the risk of TD. Also, some SOD polymorphisms may be related to the severity of TD symptoms.

6. Limitations

This study had some limitations. Firstly, our review does not include all the studies that were related to SOD. Additionally, the study did not apply meta-analysis methods in analyzing the data.

7. Suggestions for Further Studies

Future research should use a meta-analysis to further investigate the association between TD and SOD. Additional studies should demonstrate the treatment response of antioxidants using genetic methods.

Abbreviations

TD:	Tardive dyskinesia
SOD:	Superoxide dismutase
SCZ:	Schizophrenia
CuZnSOD:	Copper-zinc superoxide dismutase
AP:	Antipsychotic
ROS:	Reactive oxygen species
BD:	Bipolar disorder
OS:	Oxidative stress
PCR:	Polymerase chain reaction.

Additional Points

Key Points. Studies found an association between TD and various polymorphisms. TD-related genetic polymorphisms include MnSOD -9val and DRD3 9ser polymorphisms. TD risk is associated with altered SOD levels.

Conflicts of Interest

The authors have no conflict of interest to declare.

Acknowledgments

We thank Nathan Allen and Dave Mallpress for helping us improve the article’s quality. This work was supported by the CAS International Cooperation Research Program (153111KYSB20190004), the CAS Pioneer Hundred Talents Program, and the CAS Key Laboratory of Mental Health. Also, K.U. was supported by the Doctoral Scholarship, provided by Chinese government.

References

K. Uludag, D. M. Wang, C. Goodman, D. C. Chen, L. Wang, and X. Y. Zhang, “Prevalence, clinical correlates and risk factors associated with tardive dyskinesia in Chinese patients with schizophrenia,” Asian Journal of Psychiatry, vol. 66, 2021.
View at: Publisher Site | Google Scholar
H. J. Lee and S. G. Kang, “Genetics of tardive dyskinesia,” International Review of Neurobiology, vol. 98, pp. 231–264, 2011.
View at: Publisher Site | Google Scholar
Y. Wang, R. Branicky, A. Noë, and S. Hekimi, “Superoxide dismutases: dual roles in controlling ROS damage and regulating ROS signaling,” Journal of Cell Biology, vol. 217, no. 6, pp. 1915–1928, 2018.
View at: Publisher Site | Google Scholar
N. H. Nguyen, G.-B. Tran, and C. T. Nguyen, “Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases,” Journal of Molecular Medicine, vol. 98, no. 1, pp. 59–69, 2020.
View at: Publisher Site | Google Scholar
J. M. McCord and M. A. Edeas, “SOD, oxidative stress and human pathologies: a brief history and a future vision,” Biomedicine & Pharmacotherapy, vol. 59, no. 4, pp. 139–142, 2005.
View at: Publisher Site | Google Scholar
J. Q. Wu, Y. L. Tan, S. P. Tan et al., “Cognition impairment in schizophrenia patients with tardive dyskinesia: association with plasma superoxide dismutase activity,” Schizophrenia Research, vol. 152, no. 1, pp. 210–216, 2014.
View at: Publisher Site | Google Scholar
J. Q. Wu, Y.-L. Tan, S. Tan et al., “Association of altered CuZn superoxide dismutase and cognitive impairment in schizophrenia patients with tardive dyskinesia,” Journal of Psychiatric Research, vol. 58, pp. 167–174, 2014.
View at: Publisher Site | Google Scholar
P. Gałecki, T. Pietras, and A. Florkowki, “Pro- and antioxidant processes in schizophrenics with tardive dyskinesia,” Psychiatria Polska, vol. 39, no. 6, pp. 1131–1141, 2005.
View at: Google Scholar
K. Yamada, S. Kanba, S. Anamizu et al., “Low superoxide dismutase activity in schizophrenic patients with tardive dyskinesia,” Psychological Medicine, vol. 27, no. 5, pp. 1223–1225, 1997.
View at: Publisher Site | Google Scholar
Z. J. Zhang, X. B. Zhang, G. Hou, H. Yao, and G. P. Reynolds, “Interaction between polymorphisms of the dopamine D3 receptor and manganese superoxide dismutase genes in susceptibility to tardive dyskinesia,” Psychiatric Genetics, vol. 13, no. 3, pp. 187–192, 2003.
View at: Publisher Site | Google Scholar
Z. Zhang, G. Hou, X. Zhang, H. Yao, W. Sha, and X. Zhang, “Pharmacogenetic assessment of antipsychotic-induced tardive dyskinesia: contribution of 5-hydroxytryptamine 2C receptor gene and of a combination of dopamine D3 variant allele (Gly) and MnSOD wild allele (Val),” Zhonghua Yi Xue Yi Chuan Xue Za Zhi= Zhonghua Yixue Yichuanxue Zazhi= Chinese Journal of Medical Genetics, vol. 20, no. 2, pp. 98–102, 2003.
View at: Google Scholar
S. G. Kang, J. E. Choi, H. An et al., “Manganese superoxide dismutase gene Ala-9Val polymorphism might be related to the severity of abnormal involuntary movements in Korean schizophrenic patients,” Progress in Neuro-Psychopharmacology & Biological Psychiatry, vol. 32, no. 8, pp. 1844–1847, 2008.
View at: Publisher Site | Google Scholar
D. R. Spitz and L. W. Oberley, “Measurement of MnSOD and CuZnSOD activity in mammalian tissue homogenates,” Current Protocols in Toxicology, vol. 8, no. 1, 2001.
View at: Publisher Site | Google Scholar
Y. Oyanagui, “Reevaluation of assay methods and establishment of kit for superoxide dismutase activity,” Analytical Biochemistry, vol. 142, no. 2, pp. 290–296, 1984.
View at: Publisher Site | Google Scholar
W. A. Pryor and S. S. Godber, “Noninvasive measures of oxidative stress status in humans,” Free Radical Biology and Medicine, vol. 10, no. 3-4, pp. 177–184, 1991.
View at: Publisher Site | Google Scholar
V. Rani, S. Asthana, M. Vadhera, U. C. S. Yadav, and N. Atale, “Tools and Techniques to Measure Oxidative Stress Free Radicals in Human Health and Disease,” Free Radicals in Human Health and Disease, Springer, New Delhi, pp. 43–56, 2015.
View at: Publisher Site | Google Scholar
K. Tsuchida and M. Kobayashi, “Oxidative stress in human facial skin observed by ultraweak photon emission imaging and its correlation with biophysical properties of skin,” Scientific Reports, vol. 10, no. 1, p. 9626, 2020.
View at: Publisher Site | Google Scholar
D. Costantini and S. Verhulst, “Does high antioxidant capacity indicate low oxidative stress?” Functional Ecology, vol. 23, no. 3, pp. 506–509, 2009.
View at: Publisher Site | Google Scholar
C. P. Gonzalez-Hunt, M. Wadhwa, and L. H. Sanders, “DNA damage by oxidative stress: measurement strategies for two genomes,” Current Opinion in Toxicology, vol. 7, pp. 87–94, 2018.
View at: Publisher Site | Google Scholar
C.-U. Pae, “Additive effect between quinine oxidoreductase gene (NQO1: Pro187Ser) and manganese superoxide dismutase gene (MnSOD: Ala-9Val) polymorphisms on tardive dyskinesia in patients with schizophrenia,” Psychiatry Research, vol. 161, no. 3, pp. 336–338, 2008.
View at: Publisher Site | Google Scholar
M. Bošković, T. Vovk, M. Saje et al., “Association of SOD2, GPX1, CAT, and TNF genetic polymorphisms with oxidative stress, neurochemistry, psychopathology, and extrapyramidal symptoms in schizophrenia,” Neurochemical Research, vol. 38, no. 2, pp. 433–442, 2013.
View at: Publisher Site | Google Scholar
J. Q. Wu, D. C. Chen, Y. L. Tan, J. C. Soares, and X. Y. Zhang, “Mn-superoxide dismutase activity is associated with orofacial involuntary movements in schizophrenia patients with tardive dyskinesia,” Human Psychopharmacology: Clinical and Experimental, vol. 30, no. 1, pp. 57–63, 2015.
View at: Publisher Site | Google Scholar
M. N. Islam, A. Rauf, F. I. Fahad et al., “Superoxide dismutase: an updated review on its health benefits and industrial applications,” Critical Reviews in Food Science and Nutrition, vol. 62, no. 26, pp. 7282–7300, 2022.
View at: Publisher Site | Google Scholar
G. Bresciani, I. B. M. da Cruz, and J. González-Gallego, “Chapter four - manganese superoxide dismutase and oxidative stress modulation,” Advances in Clinical Chemistry, vol. 68, pp. 87–130, 2015.
View at: Publisher Site | Google Scholar
D. C. Owens, “Tardive dyskinesia update: treatment and management,” BJPsych Advances, vol. 25, no. 2, pp. 78–89, 2019.
View at: Publisher Site | Google Scholar
J. T. Teo, M. J. Edwards, and K. Bhatia, “Tardive dyskinesia is caused by maladaptive synaptic plasticity: a hypothesis,” Movement Disorders, vol. 27, no. 10, pp. 1205–1215, 2012.
View at: Publisher Site | Google Scholar
O. Waln and J. Jankovic, “An Update on Tardive Dyskinesia: From Phenomenology to Treatment. Tremor and Other Hyperkinetic Movements,” Tremor and Other Hyperkinetic Movements, vol. 3, 2013.
View at: Publisher Site | Google Scholar
G. N. Landis and J. Tower, “Superoxide dismutase evolution and life span regulation,” Mechanisms of Ageing and Development, vol. 126, no. 3, pp. 365–379, 2005.
View at: Publisher Site | Google Scholar
H. Zhao, R. Zhang, X. Yan, and K. Fan, “Superoxide dismutase nanozymes: an emerging star for anti-oxidation,” Journal of Materials Chemistry B, vol. 9, no. 35, pp. 6939–6957, 2021.
View at: Publisher Site | Google Scholar
C. Mao, J. Q. Yuan, Y. B. Lv et al., “Associations between superoxide dismutase, malondialdehyde and all-cause mortality in older adults: a community-based cohort study,” BMC Geriatrics, vol. 19, no. 1, p. 104, 2019.
View at: Publisher Site | Google Scholar
K. M. Powers, L. W. Oberley, and F. E. Domann, “The adventures of superoxide dismutase in health and disease: superoxide in the balance,” Oxidants in Biology, Springer, Dordrecht, pp. 183–201, 2008.
View at: Publisher Site | Google Scholar
H. Ischiropoulos and J. S. Beckman, “Oxidative stress and nitration in neurodegeneration: cause, effect, or association?” The Journal of Clinical Investigation, vol. 111, no. 2, pp. 163–169, 2003.
View at: Publisher Site | Google Scholar
Y. Zou, R. Corniola, D. Leu et al., “Extracellular superoxide dismutase is important for hippocampal neurogenesis and preservation of cognitive functions after irradiation,” Proceedings of the National Academy of Sciences, vol. 109, no. 52, pp. 21522–21527, 2012.
View at: Publisher Site | Google Scholar
R. Liu, I. Y. Liu, X. Bi et al., “Reversal of age-related learning deficits and brain oxidative stress in mice with superoxide dismutase/catalase mimetics,” Proceedings of the National Academy of Sciences, vol. 100, no. 14, pp. 8526–8531, 2003.
View at: Publisher Site | Google Scholar
E. Thiels and E. Klann, “Hippocampal memory and plasticity in superoxide dismutase mutant mice,” Physiology & Behavior, vol. 77, no. 4-5, pp. 601–605, 2002.
View at: Publisher Site | Google Scholar
L. Huo, X. Lu, F. Wu, C. Chang, Y. Ning, and X. Y. Zhang, “Elevated activity of superoxide dismutase in male late-life schizophrenia and its correlation with clinical symptoms and cognitive deficits,” BMC Psychiatry, vol. 21, no. 1, p. 606, 2021.
View at: Publisher Site | Google Scholar
K. L. Quick, S. S. Ali, R. Arch, C. Xiong, D. Wozniak, and L. L. Dugan, “A carboxyfullerene SOD mimetic improves cognition and extends the lifespan of mice,” Neurobiology of Aging, vol. 29, no. 1, pp. 117–128, 2008.
View at: Publisher Site | Google Scholar
S. Kouhestani, A. Jafari, and P. Babaei, “Kaempferol attenuates cognitive deficit via regulating oxidative stress and neuroinflammation in an ovariectomized rat model of sporadic dementia,” Neural Regeneration Research, vol. 13, no. 10, pp. 1827–1832, 2018.
View at: Publisher Site | Google Scholar
M.-S. Zhang, J.-H. Liang, M.-J. Yang et al., “Low serum superoxide dismutase is associated with a high risk of cognitive impairment after mild acute ischemic stroke,” Frontiers in Aging Neuroscience, vol. 14, 2022.
View at: Publisher Site | Google Scholar
C. Miodownik and V. Lerner, “Antioxidants as a treatment of tardive movement disorders tardive dyskinesia,” Tardive Dyskinesia: Current Approach, Nova Science Publishers, Inc., pp. 149–188, 2018.
View at: Google Scholar
X. Y. Zhang, W.-F. Zhang, D.-F. Zhou et al., “Brain-derived neurotrophic factor levels and its Val66Met gene polymorphism predict tardive dyskinesia treatment response to Ginkgo biloba,” Biological Psychiatry, vol. 72, no. 8, pp. 700–706, 2012.
View at: Publisher Site | Google Scholar
V.-L. Truong, M. Jun, and W.-S. Jeong, “Role of resveratrol in regulation of cellular defense systems against oxidative stress,” BioFactors, vol. 44, no. 1, pp. 36–49, 2018.
View at: Publisher Site | Google Scholar
H. Liu, C. Wang, P. H. Chen et al., “Association of the manganese superoxide dismutase gene Ala-9Val polymorphism with clinical phenotypes and tardive dyskinesia in schizophrenic patients,” Progress in Neuro-Psychopharmacology & Biological Psychiatry, vol. 34, no. 4, pp. 692–696, 2010.
View at: Publisher Site | Google Scholar
X. Y. Zhang, D. F. Zhou, L. Y. Cao, C. Q. Xu, and G. Y. Wu, “The effect of vitamin E treatment on tardive dyskinesia and blood superoxide dismutase: a double-blind placebo-controlled trial,” Journal of Clinical Psychopharmacology, vol. 24, no. 1, pp. 83–86, 2004.
View at: Publisher Site | Google Scholar
J. M. Su, Y. L. Tan, and D. F. Zhou, “Relationship between tardive dyskinesia and the polymorphism of superoxide dismutase val9Ala and efficacy of Chaihu Taoren capsules on it,” Zhongguo Zhong Xi Yi Jie He Za Zhi Zhongguo Zhongxiyi Jiehe Zazhi= Chinese Journal of Integrated Traditional and Western Medicine, vol. 27, no. 8, pp. 700–703, 2007.
View at: Google Scholar
G. Tsai, D. C. Goff, R. W. Chang, J. Flood, L. Baer, and J. T. Coyle, “Markers of glutamatergic neurotransmission and oxidative stress associated with tardive dyskinesia,” American Journal of Psychiatry, vol. 155, no. 9, pp. 1207–1213, 1998.
View at: Publisher Site | Google Scholar
A. Hitzeroth, D. J. Niehaus, L. Koen, W. C. Botes, J. F. Deleuze, and L. Warnich, “Association between the MnSOD Ala-9Val polymorphism and development of schizophrenia and abnormal involuntary movements in the Xhosa population,” Progress in Neuro-Psychopharmacology & Biological Psychiatry, vol. 31, no. 3, pp. 664–672, 2007.
View at: Publisher Site | Google Scholar
A. F. Y. Al Hadithy, S. A. Ivanova, P. Pechlivanoglou et al., “Missense polymorphisms in three oxidative-stress enzymes (GSTP1, SOD2, and GPX1) and dyskinesias in Russian psychiatric inpatients from Siberia,” Human Psychopharmacology, vol. 25, no. 1, pp. 84–91, 2010.
View at: Publisher Site | Google Scholar

Copyright

Copyright © 2022 Kadir Uludag et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

PDF Download Citation

Download other formats

Order printed copies

Views

546

Downloads

478

Citations