{"id":4141,"date":"2026-04-10T05:10:13","date_gmt":"2026-04-10T05:10:13","guid":{"rendered":"https:\/\/ifx0.com\/?p=4141"},"modified":"2026-04-10T05:10:14","modified_gmt":"2026-04-10T05:10:14","slug":"tardive-dyskinesia-development-superoxide-dismutase-levels-and-relevant-genetic-polymorphisms-commentary-on-importance-of-genetic-information-to-predict-td-occurrence","status":"publish","type":"post","link":"https:\/\/ifx0.com\/index.php\/2026\/04\/10\/tardive-dyskinesia-development-superoxide-dismutase-levels-and-relevant-genetic-polymorphisms-commentary-on-importance-of-genetic-information-to-predict-td-occurrence\/","title":{"rendered":"Tardive Dyskinesia Development, Superoxide Dismutase Levels, and Relevant Genetic Polymorphisms commentary on importance of genetic information to predict TD occurrence"},"content":{"rendered":"\n

Abstract<\/h2>\n
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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<\/i>. A PubMed search was used to search relevant articles using the following keywords: \u201cTardive Dyskinesia and Superoxide Dismutase\u201d. Fifty-eight articles were retrieved. Among them, 16 were included in this review. Results<\/i>. 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<\/i>. 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.<\/p>\n<\/div>\n

Uludag, K., Wang, D. M., & Zhang, X. Y. (2022). Tardive dyskinesia development, superoxide dismutase levels, and relevant genetic polymorphisms. Oxidative Medicine and Cellular Longevity<\/i>, 2022<\/i>(1), 5748924.<\/p>\n

https:\/\/onlinelibrary.wiley.com\/doi\/full\/10.1155\/2022\/5748924<\/a><\/p>\n

commentary:<\/p>\n

Commentary: Genetic Information as a Predictive Tool for Tardive Dyskinesia \u2013 The Role of Superoxide Dismutase Polymorphisms<\/h2>\n

Tardive dyskinesia (TD) remains a debilitating, often irreversible movement disorder induced by chronic antipsychotic treatment. Despite decades of research, clinicians lack reliable biomarkers to predict which patients will develop TD before irreversible symptoms appear. The accumulating evidence linking TD to oxidative stress \u2013 and specifically to superoxide dismutase (SOD) activity and its genetic variants \u2013 offers a promising avenue for risk stratification.<\/p>\n

The oxidative stress hypothesis of TD<\/strong> posits that antipsychotics, particularly first\u2011generation agents, increase free radical production in the basal ganglia. SOD is a critical first\u2011line antioxidant enzyme that converts superoxide radicals to hydrogen peroxide. Reduced SOD activity has been consistently observed in TD patients, suggesting that impaired antioxidant capacity leaves vulnerable neurons susceptible to oxidative damage.<\/p>\n

Genetic polymorphisms in SOD genes<\/strong> (e.g., SOD1<\/em>, SOD2<\/em>, and SOD3<\/em>) have been associated with altered enzyme activity and TD susceptibility. The most studied variant, SOD2<\/em> Val16Ala (rs4880), affects mitochondrial SOD activity: the Ala allele confers higher activity but may also increase hydrogen peroxide accumulation, a double\u2011edged sword. Meta\u2011analyses have reported significant, albeit modest, associations between the SOD2<\/em> Ala allele and TD risk in specific ethnic groups. Other variants, such as SOD1<\/em> rs2070424 and SOD3<\/em> rs2536512, have shown preliminary associations but require replication.<\/p>\n

Why genetic prediction matters clinically<\/strong>:<\/p>\n

    \n
  1. \n

    Pre\u2011emptive risk assessment<\/strong> \u2013 If a patient carries high\u2011risk SOD polymorphisms, clinicians could consider lower\u2011risk antipsychotics (e.g., second\u2011generation agents with lower TD liability), adjunctive antioxidants (e.g., vitamin E, N\u2011acetylcysteine), or more frequent TD monitoring.<\/p>\n<\/li>\n

  2. \n

    Personalising treatment duration<\/strong> \u2013 Genetic risk information might justify earlier antipsychotic rotation or use of clozapine (which has low TD risk) in genetically susceptible individuals.<\/p>\n<\/li>\n

  3. \n

    Mechanistic insights<\/strong> \u2013 SOD polymorphisms point to a specific pathological pathway. This encourages trials of targeted antioxidants or agents that modulate mitochondrial oxidative stress in high\u2011genetic\u2011risk subgroups.<\/p>\n<\/li>\n<\/ol>\n

    Challenges and future directions<\/strong>:<\/p>\n