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Tardive Dyskinesia Development, Superoxide Dismutase Levels, and Relevant Genetic Polymorphisms
Kadir Uludag1, Dong Mei Wang1, Xiang Yang Zhang1
1CAS Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing, China.
Oxidative Medicine and Cellular Longevity
|November 7, 2022
Summary
Genetic factors like superoxide dismutase (SOD) and DRD3 9ser influence tardive dyskinesia (TD) risk in schizophrenia patients. Altered SOD levels and specific gene variations are linked to TD development.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Tardive dyskinesia (TD) is a movement disorder common in schizophrenia (SCZ) patients with prolonged antipsychotic (AP) exposure.
- Genetic predispositions are suspected in TD development, with specific polymorphisms implicated.
Purpose of the Study:
- To review genetic polymorphisms associated with tardive dyskinesia (TD) risk.
- To investigate the role of superoxide dismutase (SOD) and other genetic factors in TD.
Main Methods:
- A systematic PubMed search was conducted using keywords: "Tardive Dyskinesia and Superoxide Dismutase".
- 16 relevant articles were selected from 58 retrieved studies for this review.
Main Results:
- Most reviewed studies focused on the association between TD and SOD-related polymorphisms.
- Previous research indicates links between TD occurrence and other genetic variations, including VAL 66 Met and DRD3 9ser.
Conclusions:
- Altered superoxide dismutase (SOD) levels are associated with an increased risk of tardive dyskinesia (TD).
- Specific genetic polymorphisms, such as VAL 66 Met and DRD3 9ser, are implicated in the risk of developing TD.
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