Tardive Dyskinesia Development, Superoxide Dismutase Levels, and Relevant Genetic Polymorphisms commentary on manuscript focusing on prediction models

Critical Commentary

Strengths:

1. Timely and Relevant: The review addresses a critical clinical problem (TD) by investigating the oxidative stress hypothesis, which remains a leading theory in the field.

2. Integration of Levels: The manuscript successfully bridges the gap between genetic data (polymorphisms) and phenotypic data (serum enzyme activity and clinical symptoms).

3. Acknowledgment of Heterogeneity: The authors openly acknowledge the difficulty in comparing studies due to differences in patient demographics, methodologies, and study designs (Section 4). They also fairly present conflicting data (e.g., [12], [43]).

   1. Clinical Implications: By discussing antioxidant treatments, the review provides a translational perspective, linking lab findings to potential therapeutic intervention

   2. Suggestions for Future Research

   3. Polygenic Risk Scores (PRS): Instead of looking at single polymorphisms (MnSOD, DRD3, HTR2C) in isolation, future studies should construct polygenic risk scores that combine variants from the entire oxidative stress pathway (SOD, CAT, GPX, NQO1) to predict TD vulnerability

 link of study:

https://onlinelibrary.wiley.com/doi/full/10.1155/2022/5748924