Publication

No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia

Levchenko, A., Vyalova, N., Pozhidaev, I. V., Boiko, A. S., Osmanova, D. Z., Fedorenko, O. Y., Semke, A. V., Bokhan, N. A., Wilffert, B., Loonen, A. J. M. & Ivanova, S. A., 8-Jan-2019, In : Human Psychopharmacology. 34, 1, e2685.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Levchenko, A., Vyalova, N., Pozhidaev, I. V., Boiko, A. S., Osmanova, D. Z., Fedorenko, O. Y., ... Ivanova, S. A. (2019). No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia. Human Psychopharmacology, 34(1), [e2685]. https://doi.org/10.1002/hup.2685

Author

Levchenko, Anastasia ; Vyalova, Natalya ; Pozhidaev, Ivan V ; Boiko, Anastasiia S ; Osmanova, Diana Z ; Fedorenko, Olga Yu ; Semke, Arkadiy V ; Bokhan, Nikolay A ; Wilffert, Bob ; Loonen, Anton J M ; Ivanova, Svetlana A. / No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia. In: Human Psychopharmacology. 2019 ; Vol. 34, No. 1.

Harvard

Levchenko, A, Vyalova, N, Pozhidaev, IV, Boiko, AS, Osmanova, DZ, Fedorenko, OY, Semke, AV, Bokhan, NA, Wilffert, B, Loonen, AJM & Ivanova, SA 2019, 'No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia' Human Psychopharmacology, vol. 34, no. 1, e2685. https://doi.org/10.1002/hup.2685

Standard

No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia. / Levchenko, Anastasia; Vyalova, Natalya; Pozhidaev, Ivan V; Boiko, Anastasiia S; Osmanova, Diana Z; Fedorenko, Olga Yu; Semke, Arkadiy V; Bokhan, Nikolay A; Wilffert, Bob; Loonen, Anton J M; Ivanova, Svetlana A.

In: Human Psychopharmacology, Vol. 34, No. 1, e2685, 08.01.2019.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Levchenko A, Vyalova N, Pozhidaev IV, Boiko AS, Osmanova DZ, Fedorenko OY et al. No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia. Human Psychopharmacology. 2019 Jan 8;34(1). e2685. https://doi.org/10.1002/hup.2685


BibTeX

@article{ecab94bcc22b444aa4032739d120bad5,
title = "No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia",
abstract = "OBJECTIVE: AKT1 and GSK3B take part in one of the intracellular cascades activated by the D2 dopamine receptor (DRD2). This receptor is antagonized by antipsychotics and plays a role in the pathogenesis of antipsychotic-induced tardive dyskinesia (TD). The present study investigated association of several polymorphisms in the two candidate genes, AKT1 and GSK3B, with TD in antipsychotic-treated patients with schizophrenia.METHODS: DNA samples from 449 patients from several Siberian regions (Russia) were genotyped, and the results were analyzed using chi-squared tests and analyses of variance.RESULTS: Antipsychotic-induced TD was not associated with either of the tested functional polymorphisms (rs334558, rs1130214, and rs3730358).CONCLUSIONS: Despite regulation of AKT1 and GSK3B by DRD2, we found no evidence that these two kinases play a major role in the pathogenesis of antipsychotic-induced TD. These results agree with previously published data and necessitate further exploration of other pathogenic mechanisms, such as neurotoxicity due to excessive dopamine metabolism.",
author = "Anastasia Levchenko and Natalya Vyalova and Pozhidaev, {Ivan V} and Boiko, {Anastasiia S} and Osmanova, {Diana Z} and Fedorenko, {Olga Yu} and Semke, {Arkadiy V} and Bokhan, {Nikolay A} and Bob Wilffert and Loonen, {Anton J M} and Ivanova, {Svetlana A}",
note = "{\circledC} 2019 John Wiley & Sons, Ltd.",
year = "2019",
month = "1",
day = "8",
doi = "10.1002/hup.2685",
language = "English",
volume = "34",
journal = "Human Psychopharmacology",
issn = "0885-6222",
publisher = "John Wiley and Sons Ltd",
number = "1",

}

RIS

TY - JOUR

T1 - No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia

AU - Levchenko, Anastasia

AU - Vyalova, Natalya

AU - Pozhidaev, Ivan V

AU - Boiko, Anastasiia S

AU - Osmanova, Diana Z

AU - Fedorenko, Olga Yu

AU - Semke, Arkadiy V

AU - Bokhan, Nikolay A

AU - Wilffert, Bob

AU - Loonen, Anton J M

AU - Ivanova, Svetlana A

N1 - © 2019 John Wiley & Sons, Ltd.

PY - 2019/1/8

Y1 - 2019/1/8

N2 - OBJECTIVE: AKT1 and GSK3B take part in one of the intracellular cascades activated by the D2 dopamine receptor (DRD2). This receptor is antagonized by antipsychotics and plays a role in the pathogenesis of antipsychotic-induced tardive dyskinesia (TD). The present study investigated association of several polymorphisms in the two candidate genes, AKT1 and GSK3B, with TD in antipsychotic-treated patients with schizophrenia.METHODS: DNA samples from 449 patients from several Siberian regions (Russia) were genotyped, and the results were analyzed using chi-squared tests and analyses of variance.RESULTS: Antipsychotic-induced TD was not associated with either of the tested functional polymorphisms (rs334558, rs1130214, and rs3730358).CONCLUSIONS: Despite regulation of AKT1 and GSK3B by DRD2, we found no evidence that these two kinases play a major role in the pathogenesis of antipsychotic-induced TD. These results agree with previously published data and necessitate further exploration of other pathogenic mechanisms, such as neurotoxicity due to excessive dopamine metabolism.

AB - OBJECTIVE: AKT1 and GSK3B take part in one of the intracellular cascades activated by the D2 dopamine receptor (DRD2). This receptor is antagonized by antipsychotics and plays a role in the pathogenesis of antipsychotic-induced tardive dyskinesia (TD). The present study investigated association of several polymorphisms in the two candidate genes, AKT1 and GSK3B, with TD in antipsychotic-treated patients with schizophrenia.METHODS: DNA samples from 449 patients from several Siberian regions (Russia) were genotyped, and the results were analyzed using chi-squared tests and analyses of variance.RESULTS: Antipsychotic-induced TD was not associated with either of the tested functional polymorphisms (rs334558, rs1130214, and rs3730358).CONCLUSIONS: Despite regulation of AKT1 and GSK3B by DRD2, we found no evidence that these two kinases play a major role in the pathogenesis of antipsychotic-induced TD. These results agree with previously published data and necessitate further exploration of other pathogenic mechanisms, such as neurotoxicity due to excessive dopamine metabolism.

U2 - 10.1002/hup.2685

DO - 10.1002/hup.2685

M3 - Article

VL - 34

JO - Human Psychopharmacology

JF - Human Psychopharmacology

SN - 0885-6222

IS - 1

M1 - e2685

ER -

ID: 73833058