Clement C Zai1,2,3, Arun K Tiwari1,2, Nabilah I Chowdhury1, Zeynep Yilmaz1,4, Vincenzo de Luca1,2,5, Daniel J Müller1,2,5, Steven G Potkin6, Jeffrey A Lieberman7, Herbert Y Meltzer8, Aristotle N Voineskos1,2,5, Gary Remington2,5, James L Kennedy1,2,5. 1. a Neurogenetics Section, Tanenbaum Centre for Pharmacogenetics, Molecular Brain Science , Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health , Toronto , ON , Canada. 2. b Department of Psychiatry , University of Toronto , Toronto , ON , Canada. 3. c Laboratory Medicine and Pathophysiology , University of Toronto , ON , Canada. 4. d Center of Excellence for Eating Disorders at the University of North Carolina at Chapel Hill , NC , USA. 5. e Institute of Medical Science , University of Toronto , Toronto , ON , Canada. 6. f Department of Psychiatry and Human Behavior , University of California , Irvine, Irvine , CA , USA. 7. g Department of Psychiatry , Columbia University College of Physicians and Surgeons , NY , USA. 8. h Psychiatry and Behavioral Sciences, Pharmacology and Physiology, Chemistry of Life Processes Institute , Northwestern University Feinberg School of Medicine , Chicago , IL , USA.
Abstract
OBJECTIVES: Tardive dyskinesia (TD) is a movement disorder that may develop as a side effect of antipsychotic medication. The aetiology underlying TD is unclear, but a number of mechanisms have been proposed. METHODS: We investigated single-nucleotide polymorphisms (SNPs) in the genes coding for neuregulin-1 and erbB-4 receptor in our sample of 153 European schizophrenia patients for possible association with TD. RESULTS: We found the ERBB4 rs839523 CC genotype to be associated with risk for TD occurrence and increased severity as measured by the Abnormal Involuntary Movement Scale (AIMS) (P = .003). CONCLUSIONS: This study supports a role for the neuregulin signalling pathway in TD, although independent replications are warranted.
OBJECTIVES:Tardive dyskinesia (TD) is a movement disorder that may develop as a side effect of antipsychotic medication. The aetiology underlying TD is unclear, but a number of mechanisms have been proposed. METHODS: We investigated single-nucleotide polymorphisms (SNPs) in the genes coding for neuregulin-1 and erbB-4 receptor in our sample of 153 European schizophreniapatients for possible association with TD. RESULTS: We found the ERBB4rs839523 CC genotype to be associated with risk for TD occurrence and increased severity as measured by the Abnormal Involuntary Movement Scale (AIMS) (P = .003). CONCLUSIONS: This study supports a role for the neuregulin signalling pathway in TD, although independent replications are warranted.
Authors: Clement C Zai; Frankie H Lee; Arun K Tiwari; Justin Y Lu; Vincenzo de Luca; Miriam S Maes; Deanna Herbert; Anashe Shahmirian; Sheraz Y Cheema; Gwyneth C Zai; Anupama Atukuri; Michael Sherman; Sajid A Shaikh; Maria Tampakeras; Natalie Freeman; Nicole King; Daniel J Müller; Lior Greenbaum; Bernard Lerer; Aristotle N Voineskos; Steven G Potkin; Jeffrey A Lieberman; Herbert Y Meltzer; Gary Remington; James L Kennedy Journal: Front Pharmacol Date: 2018-09-18 Impact factor: 5.810