Publication

Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia

Ivanova, S. A., Geers, L. M., Al Hadithy, A. F. Y., Pechlivanoglou, P., Semke, A. V., Vyalova, N. M., Rudikov, E. V., Fedorenko, O. Y., Wilffert, B., Bokhan, N. A., Brouwers, J. R. B. J. & Loonen, A. J. M., 3-Apr-2014, In : Progress in Neuro-Psychopharmacology & Biological Psychiatry. 50, p. 172-177 6 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Ivanova, S. A., Geers, L. M., Al Hadithy, A. F. Y., Pechlivanoglou, P., Semke, A. V., Vyalova, N. M., ... Loonen, A. J. M. (2014). Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 50, 172-177. https://doi.org/10.1016/j.pnpbp.2013.12.015

Author

Ivanova, Svetlana A. ; Geers, Lisanne M. ; Al Hadithy, Asmar F.Y. ; Pechlivanoglou, Petros ; Semke, Arkadiy V. ; Vyalova, Natalia M. ; Rudikov, Evgeniy V. ; Fedorenko, Olga Y. ; Wilffert, Bob ; Bokhan, Nikolay A. ; Brouwers, Jacobus R.B.J. ; Loonen, Anton J.M. / Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia. In: Progress in Neuro-Psychopharmacology & Biological Psychiatry. 2014 ; Vol. 50. pp. 172-177.

Harvard

Ivanova, SA, Geers, LM, Al Hadithy, AFY, Pechlivanoglou, P, Semke, AV, Vyalova, NM, Rudikov, EV, Fedorenko, OY, Wilffert, B, Bokhan, NA, Brouwers, JRBJ & Loonen, AJM 2014, 'Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia' Progress in Neuro-Psychopharmacology & Biological Psychiatry, vol. 50, pp. 172-177. https://doi.org/10.1016/j.pnpbp.2013.12.015

Standard

Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia. / Ivanova, Svetlana A.; Geers, Lisanne M.; Al Hadithy, Asmar F.Y.; Pechlivanoglou, Petros; Semke, Arkadiy V.; Vyalova, Natalia M.; Rudikov, Evgeniy V.; Fedorenko, Olga Y.; Wilffert, Bob; Bokhan, Nikolay A.; Brouwers, Jacobus R.B.J.; Loonen, Anton J.M.

In: Progress in Neuro-Psychopharmacology & Biological Psychiatry, Vol. 50, 03.04.2014, p. 172-177.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Ivanova SA, Geers LM, Al Hadithy AFY, Pechlivanoglou P, Semke AV, Vyalova NM et al. Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia. Progress in Neuro-Psychopharmacology & Biological Psychiatry. 2014 Apr 3;50:172-177. https://doi.org/10.1016/j.pnpbp.2013.12.015


BibTeX

@article{c1e31605854845da9efe432b52c705fd,
title = "Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia",
abstract = "Background: Tardive dyskinesia (TD) is a potentially irreversible consequence of long term treatment with antipsychotic drugs which is according to a well-known theory believed to be related to oxidative stress induced neurotoxicity. Dehydroepiandrosterone (DHEA) is an endogenous antioxidant with neuroprotective activity. The biosynthesis of DHEA depends upon the activity of cytochrome P450c17 alpha (CYP17). The gene that encodes for CYP17 has a (T34C) single nucleotide polymorphism which enhances CYP17 transcription and expression.Objective: To test the hypothesis that carriership of a more active CYP17 variant would result in higher DHEA(S) levels and protect against neurotoxicity which results in orofaciolingual TD (TDof), limb-truncal TD (TDlt) or both (TDsum).Method: Tardive dyskinesia was assessed cross-sectionally in 146 Caucasian psychiatric inpatients from Siberia.Results: Patients who are carriers of the Cyp17 genotype CC have less chance of developing TD compared to patients who are carriers of the Cyp17 genotypes TC or TT (p <0.05). However, these carriers have significant lower circulating DHEAS levels compared to carriers of the Cyp17 genotypes TC and TT (p <0.05). Conversely, carriers of the CYP17 T-allele have significant elevated DHEAS levels. After correcting for gender and age no significant relationship between Cyp17 genotype CC, the T-allelle and the C-allele and the DHEAS concentration of patients was observed.Conclusions: Although an association between the CYP17 CC genotype and TD is indicated, our findings do not support the hypothesis that this is mediated through increased DHEA(S) levels. We believe that the relationship between this polymorphism and neuroprotective effects of steroids is more complex and cannot be elucidated without taking the posttranslational regulation of the enzyme into account. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.",
keywords = "Cyp17, Dehydroepiandrosterone, Tardive dyskinesia, cytochrome P450 family 17, prasterone sulfate, article, biosynthesis, blood level, blood sampling, clinical effectiveness, clinical feature, controlled study, CYP17 gene, disease activity, disease association, disease severity, drug efficacy, female, gene, gene frequency, gene function, gene identification, genetic polymorphism, genetic variability, genotype, hormone action, human, major clinical study, male, molecular pathology, neuroprotection, neurotoxicity, outcome assessment, patient assessment, scoring system, sex hormone determination, tardive dyskinesia",
author = "Ivanova, {Svetlana A.} and Geers, {Lisanne M.} and {Al Hadithy}, {Asmar F.Y.} and Petros Pechlivanoglou and Semke, {Arkadiy V.} and Vyalova, {Natalia M.} and Rudikov, {Evgeniy V.} and Fedorenko, {Olga Y.} and Bob Wilffert and Bokhan, {Nikolay A.} and Brouwers, {Jacobus R.B.J.} and Loonen, {Anton J.M.}",
year = "2014",
month = "4",
day = "3",
doi = "10.1016/j.pnpbp.2013.12.015",
language = "English",
volume = "50",
pages = "172--177",
journal = "Progress in Neuro-Psychopharmacology & Biological Psychiatry",
issn = "1878-4216",
publisher = "PERGAMON-ELSEVIER SCIENCE LTD",

}

RIS

TY - JOUR

T1 - Dehydroepiandrosterone sulphate as a putative protective factor against tardive dyskinesia

AU - Ivanova, Svetlana A.

AU - Geers, Lisanne M.

AU - Al Hadithy, Asmar F.Y.

AU - Pechlivanoglou, Petros

AU - Semke, Arkadiy V.

AU - Vyalova, Natalia M.

AU - Rudikov, Evgeniy V.

AU - Fedorenko, Olga Y.

AU - Wilffert, Bob

AU - Bokhan, Nikolay A.

AU - Brouwers, Jacobus R.B.J.

AU - Loonen, Anton J.M.

PY - 2014/4/3

Y1 - 2014/4/3

N2 - Background: Tardive dyskinesia (TD) is a potentially irreversible consequence of long term treatment with antipsychotic drugs which is according to a well-known theory believed to be related to oxidative stress induced neurotoxicity. Dehydroepiandrosterone (DHEA) is an endogenous antioxidant with neuroprotective activity. The biosynthesis of DHEA depends upon the activity of cytochrome P450c17 alpha (CYP17). The gene that encodes for CYP17 has a (T34C) single nucleotide polymorphism which enhances CYP17 transcription and expression.Objective: To test the hypothesis that carriership of a more active CYP17 variant would result in higher DHEA(S) levels and protect against neurotoxicity which results in orofaciolingual TD (TDof), limb-truncal TD (TDlt) or both (TDsum).Method: Tardive dyskinesia was assessed cross-sectionally in 146 Caucasian psychiatric inpatients from Siberia.Results: Patients who are carriers of the Cyp17 genotype CC have less chance of developing TD compared to patients who are carriers of the Cyp17 genotypes TC or TT (p <0.05). However, these carriers have significant lower circulating DHEAS levels compared to carriers of the Cyp17 genotypes TC and TT (p <0.05). Conversely, carriers of the CYP17 T-allele have significant elevated DHEAS levels. After correcting for gender and age no significant relationship between Cyp17 genotype CC, the T-allelle and the C-allele and the DHEAS concentration of patients was observed.Conclusions: Although an association between the CYP17 CC genotype and TD is indicated, our findings do not support the hypothesis that this is mediated through increased DHEA(S) levels. We believe that the relationship between this polymorphism and neuroprotective effects of steroids is more complex and cannot be elucidated without taking the posttranslational regulation of the enzyme into account. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.

AB - Background: Tardive dyskinesia (TD) is a potentially irreversible consequence of long term treatment with antipsychotic drugs which is according to a well-known theory believed to be related to oxidative stress induced neurotoxicity. Dehydroepiandrosterone (DHEA) is an endogenous antioxidant with neuroprotective activity. The biosynthesis of DHEA depends upon the activity of cytochrome P450c17 alpha (CYP17). The gene that encodes for CYP17 has a (T34C) single nucleotide polymorphism which enhances CYP17 transcription and expression.Objective: To test the hypothesis that carriership of a more active CYP17 variant would result in higher DHEA(S) levels and protect against neurotoxicity which results in orofaciolingual TD (TDof), limb-truncal TD (TDlt) or both (TDsum).Method: Tardive dyskinesia was assessed cross-sectionally in 146 Caucasian psychiatric inpatients from Siberia.Results: Patients who are carriers of the Cyp17 genotype CC have less chance of developing TD compared to patients who are carriers of the Cyp17 genotypes TC or TT (p <0.05). However, these carriers have significant lower circulating DHEAS levels compared to carriers of the Cyp17 genotypes TC and TT (p <0.05). Conversely, carriers of the CYP17 T-allele have significant elevated DHEAS levels. After correcting for gender and age no significant relationship between Cyp17 genotype CC, the T-allelle and the C-allele and the DHEAS concentration of patients was observed.Conclusions: Although an association between the CYP17 CC genotype and TD is indicated, our findings do not support the hypothesis that this is mediated through increased DHEA(S) levels. We believe that the relationship between this polymorphism and neuroprotective effects of steroids is more complex and cannot be elucidated without taking the posttranslational regulation of the enzyme into account. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.

KW - Cyp17

KW - Dehydroepiandrosterone

KW - Tardive dyskinesia

KW - cytochrome P450 family 17

KW - prasterone sulfate

KW - article

KW - biosynthesis

KW - blood level

KW - blood sampling

KW - clinical effectiveness

KW - clinical feature

KW - controlled study

KW - CYP17 gene

KW - disease activity

KW - disease association

KW - disease severity

KW - drug efficacy

KW - female

KW - gene

KW - gene frequency

KW - gene function

KW - gene identification

KW - genetic polymorphism

KW - genetic variability

KW - genotype

KW - hormone action

KW - human

KW - major clinical study

KW - male

KW - molecular pathology

KW - neuroprotection

KW - neurotoxicity

KW - outcome assessment

KW - patient assessment

KW - scoring system

KW - sex hormone determination

KW - tardive dyskinesia

U2 - 10.1016/j.pnpbp.2013.12.015

DO - 10.1016/j.pnpbp.2013.12.015

M3 - Article

VL - 50

SP - 172

EP - 177

JO - Progress in Neuro-Psychopharmacology & Biological Psychiatry

JF - Progress in Neuro-Psychopharmacology & Biological Psychiatry

SN - 1878-4216

ER -

ID: 13644808