Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia

Miriam S. Maes; Justin Y. Lu; Arun K. Tiwari; Natalie Freeman; Vincenzo de Luca; Daniel J. Müller; Aristotle N. Voineskos; Steven G. Potkin; Jeffrey A. Lieberman; Herbert Y. Meltzer; Gary Remington; James L. Kennedy; Clement C. Zai

doi:10.1002/ddr.21681

Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia

Miriam S. Maes, Justin Y. Lu, Arun K. Tiwari, Natalie Freeman, Vincenzo de Luca, Daniel J. Müller, Aristotle N. Voineskos, Steven G. Potkin, Jeffrey A. Lieberman, Herbert Y. Meltzer, Gary Remington, James L. Kennedy^*, Clement C. Zai

^*Corresponding author for this work

Psychiatry and Behavioral Sciences

Research output: Contribution to journal › Article

Abstract

Tardive dyskinesia (TD) is a potentially irreversible movement disorder observed following long-term antipsychotic exposure. Its cause is unknown; however, a genetic component has been supported by studies of affected families. Dysbindin-1, encoded by the dystrobrevin-binding protein 1 DTNBP1 gene, has been associated with schizophrenia and is potentially involved in dopamine neurotransmission through its regulation of dopamine release and dopamine D2 receptor recycling, making it a candidate for investigation in TD. We investigated common variants across the DTNBP1 gene in our schizophrenia/patients with schizoaffective disorder of European ancestry. We found a number of DTNBP1 three-marker haplotypes to be associated with TD occurrence and TD severity (p < 0.05). These preliminary findings, if replicated in larger independent samples, would suggest that drugs targeting dysbindin-1 may be an option in the prevention and treatment of TD.

Original language	English (US)
Journal	Drug Development Research
DOIs	https://doi.org/10.1002/ddr.21681
State	Accepted/In press - 2020

Keywords

dysbindin-1 (DTNBP1)
pharmacogenetics
schizophrenia
tardive dyskinesia (TD)

ASJC Scopus subject areas

Drug Discovery

Access to Document

10.1002/ddr.21681

Fingerprint Dive into the research topics of 'Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia'. Together they form a unique fingerprint.

Cite this

Maes, M. S., Lu, J. Y., Tiwari, A. K., Freeman, N., de Luca, V., Müller, D. J., Voineskos, A. N., Potkin, S. G., Lieberman, J. A., Meltzer, H. Y., Remington, G., Kennedy, J. L., & Zai, C. C. (Accepted/In press). Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia. Drug Development Research. https://doi.org/10.1002/ddr.21681

@article{3d3a7c958fc24bc28b6d0d210a071875,

title = "Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia",

abstract = "Tardive dyskinesia (TD) is a potentially irreversible movement disorder observed following long-term antipsychotic exposure. Its cause is unknown; however, a genetic component has been supported by studies of affected families. Dysbindin-1, encoded by the dystrobrevin-binding protein 1 DTNBP1 gene, has been associated with schizophrenia and is potentially involved in dopamine neurotransmission through its regulation of dopamine release and dopamine D2 receptor recycling, making it a candidate for investigation in TD. We investigated common variants across the DTNBP1 gene in our schizophrenia/patients with schizoaffective disorder of European ancestry. We found a number of DTNBP1 three-marker haplotypes to be associated with TD occurrence and TD severity (p < 0.05). These preliminary findings, if replicated in larger independent samples, would suggest that drugs targeting dysbindin-1 may be an option in the prevention and treatment of TD.",

keywords = "dysbindin-1 (DTNBP1), pharmacogenetics, schizophrenia, tardive dyskinesia (TD)",

author = "Maes, {Miriam S.} and Lu, {Justin Y.} and Tiwari, {Arun K.} and Natalie Freeman and {de Luca}, Vincenzo and M{\"u}ller, {Daniel J.} and Voineskos, {Aristotle N.} and Potkin, {Steven G.} and Lieberman, {Jeffrey A.} and Meltzer, {Herbert Y.} and Gary Remington and Kennedy, {James L.} and Zai, {Clement C.}",

year = "2020",

doi = "10.1002/ddr.21681",

language = "English (US)",

journal = "Drug Development Research",

issn = "0272-4391",

publisher = "John Wiley and Sons Inc.",

}

Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia. / Maes, Miriam S.; Lu, Justin Y.; Tiwari, Arun K.; Freeman, Natalie; de Luca, Vincenzo; Müller, Daniel J.; Voineskos, Aristotle N.; Potkin, Steven G.; Lieberman, Jeffrey A.; Meltzer, Herbert Y.; Remington, Gary; Kennedy, James L.; Zai, Clement C.

In: Drug Development Research, 2020.

Research output: Contribution to journal › Article

TY - JOUR

T1 - Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia

AU - Maes, Miriam S.

AU - Lu, Justin Y.

AU - Tiwari, Arun K.

AU - Freeman, Natalie

AU - de Luca, Vincenzo

AU - Müller, Daniel J.

AU - Voineskos, Aristotle N.

AU - Potkin, Steven G.

AU - Lieberman, Jeffrey A.

AU - Meltzer, Herbert Y.

AU - Remington, Gary

AU - Kennedy, James L.

AU - Zai, Clement C.

PY - 2020

Y1 - 2020

N2 - Tardive dyskinesia (TD) is a potentially irreversible movement disorder observed following long-term antipsychotic exposure. Its cause is unknown; however, a genetic component has been supported by studies of affected families. Dysbindin-1, encoded by the dystrobrevin-binding protein 1 DTNBP1 gene, has been associated with schizophrenia and is potentially involved in dopamine neurotransmission through its regulation of dopamine release and dopamine D2 receptor recycling, making it a candidate for investigation in TD. We investigated common variants across the DTNBP1 gene in our schizophrenia/patients with schizoaffective disorder of European ancestry. We found a number of DTNBP1 three-marker haplotypes to be associated with TD occurrence and TD severity (p < 0.05). These preliminary findings, if replicated in larger independent samples, would suggest that drugs targeting dysbindin-1 may be an option in the prevention and treatment of TD.

AB - Tardive dyskinesia (TD) is a potentially irreversible movement disorder observed following long-term antipsychotic exposure. Its cause is unknown; however, a genetic component has been supported by studies of affected families. Dysbindin-1, encoded by the dystrobrevin-binding protein 1 DTNBP1 gene, has been associated with schizophrenia and is potentially involved in dopamine neurotransmission through its regulation of dopamine release and dopamine D2 receptor recycling, making it a candidate for investigation in TD. We investigated common variants across the DTNBP1 gene in our schizophrenia/patients with schizoaffective disorder of European ancestry. We found a number of DTNBP1 three-marker haplotypes to be associated with TD occurrence and TD severity (p < 0.05). These preliminary findings, if replicated in larger independent samples, would suggest that drugs targeting dysbindin-1 may be an option in the prevention and treatment of TD.

KW - dysbindin-1 (DTNBP1)

KW - pharmacogenetics

KW - schizophrenia

KW - tardive dyskinesia (TD)

UR - http://www.scopus.com/inward/record.url?scp=85084453725&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85084453725&partnerID=8YFLogxK

U2 - 10.1002/ddr.21681

DO - 10.1002/ddr.21681

M3 - Article

C2 - 32394511

AN - SCOPUS:85084453725

JO - Drug Development Research

JF - Drug Development Research

SN - 0272-4391

ER -