The development of tardive dyskinesia (TD) is influenced by various factors including the type of antipsychotic, dose, duration of treatment, and individual genetic susceptibility. Studies have highlighted the role of genetic variations influencing the pharmacokinetics and pharmacodynamics of drugs, such as variations in dopamine, serotonin, and cannabinoid receptors, oxidative stress factors, and certain enzymes and transporters like CYP isoenzymes. Understanding these genetic factors is crucial as they contribute to the variability in drug metabolism and response, affecting both the efficacy and the adverse effects of antipsychotics.

Clinical and preclinical research continues to explore the complex interplay of genetics and medication effects to better understand and manage TD. Pharmacogenomics seeks to tailor medication based on genetic profiles to minimize risks and optimize treatment efficacy. However, despite the identification of potential genetic markers associated with TD risk, clinical application remains limited due to inconsistent study results and small sample sizes. Larger, more comprehensive studies are necessary to validate these findings and develop robust pharmacogenetic guidelines.

Reference: Tsermpini EE, Redenšek S, Dolžan V. Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies. Front Pharmacol. 2022;12:834129. doi: 10.3389/fphar.2021.834129.