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Published on: October 4, 2021
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A Focused Update on Tardive Dyskinesia
1Department of Stomatology, Faculty of Dental Medicine, University of Montreal, Montreal, Quebec, Canada; Department of Medicine, University of Montreal Hospital Centre (CHU Montreal), Montreal, Quebec, Canada; and Montreal Mental Health University Institute (IUSMM), Montreal, QC, Canada.
Summary
Tardive dyskinesia (TD) involves involuntary movements from antipsychotics. Research suggests dopamine D3 receptor upregulation and GSK-3β signaling may be involved, offering new treatment avenues.
Area of Science:
- Neuroscience
- Pharmacology
- Movement Disorders
Background:
- Tardive dyskinesia (TD) is a motor disorder from long-term antipsychotic use.
- Despite newer drugs, TD affects 20% of patients, impacting quality of life.
- The molecular basis of TD remains unclear, complicating management.
Purpose of the Study:
- To investigate the neurobiological underpinnings of tardive dyskinesia.
- To re-evaluate the dopamine D2 receptor supersensitivity hypothesis in TD.
- To explore potential molecular targets for TD treatment.
Main Methods:
- Utilized an experimental nonhuman primate model of antipsychotic-induced dyskinesia.
- Analyzed receptor expression in the striatum of dyskinetic versus control animals.
- Examined signaling pathways, including glycogen synthase kinase-3β (GSK-3β).
Main Results:
- Found significant upregulation of dopamine D3 receptors, not D2, in dyskinetic primates.
- Observed indirect evidence linking GSK-3β overactivation to TD.
- New VMAT2 inhibitors show promise for TD management.
Conclusions:
- Dopamine D3 receptor upregulation may be more critical than D2 in TD pathogenesis.
- GSK-3β signaling is a potential contributor to TD development.
- Emerging treatments and algorithms offer improved TD management strategies.
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