Likelihood of mechanistic roles for dopaminergic, serotonergic and glutamatergic receptors in tardive dyskinesia: A comparison of genetic variants in two independent patient populations; SAGE Open Medicine; Vol. 4

Detalles Bibliográficos
Parent link:SAGE Open Medicine
Vol. 4.— 2016.— [9 p.]
Autor Corporativo: Национальный исследовательский Томский политехнический университет (ТПУ) Институт неразрушающего контроля (ИНК) Кафедра экологии и безопасности жизнедеятельности (ЭБЖ)
Otros Autores: Ivanova S. A. Svetlana Aleksandrovna, Loonen A. J. Anton, Bakker N. R., Freydin M. V., Woerds N. J., Hadithy A. FY Al. Asmar, Semke A. V. Arkady Valentinovich, Fedorenko O. Yu. Olga Yurievna, Brouwers J. RBJ Jacobus, Bokhan N. A. Nikolay Aleksandrovich, Jim van Os, Peter N van Harten, Wilffert B. Bob
Sumario:Title screen
An established theory for the pathogenesis of tardive dyskinesia is disturbed dopaminergic receptor sensitivity and/or dopaminergic intracellular signaling. We examined associations between genetic variants of neurotransmitter receptors and tardive dyskinesia. Methods: We assessed tardive dyskinesia in Caucasian psychiatric inpatients from Siberia (N = 431) and a long-stay population from the Netherlands (N = 168). These patients were genotyped for 43 tag single nucleotide polymorphisms in five neurotransmitter receptor genes, and the results for the two populations were compared. Results: Several significant associations with tardive dyskinesia were identified, but only GRIN2A (rs1345423) was found in both patient populations. This lack of agreement was probably due to the small effect size of the associations, the multiple testing and the small sample size of the Dutch patient population. After reviewing the literature, we propose that the constitutive stimulatory activity of serotonergic type 2 receptors may be relevant. Conclusions: Inactivity of the serotonergic, type 2C receptor or blockade of these receptors by atypical antipsychotic drugs may decrease the vulnerability to develop tardive dyskinesia.
Lenguaje:inglés
Publicado: 2016
Materias:
Acceso en línea:http://dx.doi.org/10.1177/2050312116643673
Formato: Electrónico Capítulo de libro
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=654132

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200 1 |a Likelihood of mechanistic roles for dopaminergic, serotonergic and glutamatergic receptors in tardive dyskinesia: A comparison of genetic variants in two independent patient populations  |f S. A. Ivanova [et al.] 
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300 |a Title screen 
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330 |a An established theory for the pathogenesis of tardive dyskinesia is disturbed dopaminergic receptor sensitivity and/or dopaminergic intracellular signaling. We examined associations between genetic variants of neurotransmitter receptors and tardive dyskinesia. Methods: We assessed tardive dyskinesia in Caucasian psychiatric inpatients from Siberia (N = 431) and a long-stay population from the Netherlands (N = 168). These patients were genotyped for 43 tag single nucleotide polymorphisms in five neurotransmitter receptor genes, and the results for the two populations were compared. Results: Several significant associations with tardive dyskinesia were identified, but only GRIN2A (rs1345423) was found in both patient populations. This lack of agreement was probably due to the small effect size of the associations, the multiple testing and the small sample size of the Dutch patient population. After reviewing the literature, we propose that the constitutive stimulatory activity of serotonergic type 2 receptors may be relevant. Conclusions: Inactivity of the serotonergic, type 2C receptor or blockade of these receptors by atypical antipsychotic drugs may decrease the vulnerability to develop tardive dyskinesia. 
461 |t SAGE Open Medicine 
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