Association Study Indicates a Protective Role of Phosphatidylinositol-4-phosphate-5-kinase Against Tardive Dyskinesia

Overview

Journal Int J Neuropsychopharmacol

Publisher Oxford University Press

Specialty Psychiatry

Date 2014 Dec 31

PMID 25548108

Citations 11

Authors

Olga Yu Fedorenko

Anton J M Loonen

Florian Lang

Valentina A Toshchakova

Evgenia G Boyarko

Arkadiy V Semke

Nikolay a Bokhan

Nikolay V Govorin

Lyubomir I Aftanas

Svetlana A Ivanova

Affiliations

Soon will be listed here.

Abstract

Background: Tardive dyskinesia is a disorder characterized by involuntary muscle movements that occur as a complication of long-term treatment with antipsychotic drugs. It has been suggested to be related to a malfunctioning of the indirect pathway of the motor part of the cortical-striatal-thalamic-cortical circuit, which may be caused by oxidative stress-induced neurotoxicity.

Methods: The purpose of our study was to investigate the possible association between phosphatidylinositol-4-phosphate-5-kinase type IIa (PIP5K2A) function and tardive dyskinesia in 491 Caucasian patients with schizophrenia from 3 different psychiatric institutes in West Siberia. The Abnormal Involuntary Movement Scale was used to assess tardive dyskinesia. Individuals were genotyped for 3 single nucleotide polymorphisms in PIP5K2A gene: rs10828317, rs746203, and rs8341.

Results: A significant association was established between the functional mutation N251S-polymorphism of the PIP5K2A gene (rs10828317) and tardive dyskinesia, while the other 2 examined nonfunctional single nucleotide polymorphisms were not related.

Conclusions: We conclude from this association that PIP5K2A is possibly involved in a mechanism protecting against tardive dyskinesia-inducing neurotoxicity. This corresponds to our hypothesis that tardive dyskinesia is related to neurotoxicity at striatal indirect pathway medium-sized spiny neurons.

Citing Articles

Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies.

Tsermpini E, Redensek S, Dolzan V Front Pharmacol. 2022; 12:834129.

PMID: 35140610 PMC: 8819690. DOI: 10.3389/fphar.2021.834129.

Tardive Dyskinesia in Older Persons Taking Antipsychotics.

Citrome L, Isaacson S, Larson D, Kremens D Neuropsychiatr Dis Treat. 2021; 17:3127-3134.

PMID: 34703232 PMC: 8524363. DOI: 10.2147/NDT.S328301.

Association of Polymorphisms with Alcohol Use Disorder.

Fedorenko O, Mikhalitskaya E, Toshchakova V, Loonen A, Bokhan N, Ivanova S Genes (Basel). 2021; 12(10).

PMID: 34681036 PMC: 8535504. DOI: 10.3390/genes12101642.

Genome wide study of tardive dyskinesia in schizophrenia.

Lim K, Lam M, Zai C, Tay J, Karlsson N, Deshpande S Transl Psychiatry. 2021; 11(1):351.

PMID: 34103471 PMC: 8187404. DOI: 10.1038/s41398-021-01471-y.

, , and as Potential Candidate Biomarker Genes for Several Clinical Subphenotypes of Depression and Bipolar Disorder.

Levchenko A, Vyalova N, Nurgaliev T, Pozhidaev I, Simutkin G, Bokhan N Front Genet. 2020; 11:936.

PMID: 33193575 PMC: 7478333. DOI: 10.3389/fgene.2020.00936.

References

Glazer W . Review of incidence studies of tardive dyskinesia associated with typical antipsychotics. J Clin Psychiatry. 2000; 61 Suppl 4:15-20. View

Seebohm G, Wrobel E, Pusch M, Dicks M, Terhag J, Matschke V . Structural basis of PI(4,5)P2-dependent regulation of GluA1 by phosphatidylinositol-5-phosphate 4-kinase, type II, alpha (PIP5K2A). Pflugers Arch. 2014; 466(10):1885-97. PMC: 4159565. DOI: 10.1007/s00424-013-1424-8. View

Schooler N, Kane J . Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry. 1982; 39(4):486-7. DOI: 10.1001/archpsyc.1982.04290040080014. View

Kane J, Woerner M, Lieberman J . Tardive dyskinesia: prevalence, incidence, and risk factors. J Clin Psychopharmacol. 1988; 8(4 Suppl):52S-56S. View

Margolese H, Chouinard G, Kolivakis T, Beauclair L, Miller R . Tardive dyskinesia in the era of typical and atypical antipsychotics. Part 1: pathophysiology and mechanisms of induction. Can J Psychiatry. 2005; 50(9):541-7. DOI: 10.1177/070674370505000907. View

Kane J . Tardive dyskinesia circa 2006. Am J Psychiatry. 2006; 163(8):1316-8. DOI: 10.1176/ajp.2006.163.8.1316. View

Schwab S, Knapp M, Sklar P, Eckstein G, Sewekow C, Borrmann-Hassenbach M . Evidence for association of DNA sequence variants in the phosphatidylinositol-4-phosphate 5-kinase IIalpha gene (PIP5K2A) with schizophrenia. Mol Psychiatry. 2006; 11(9):837-46. DOI: 10.1038/sj.mp.4001864. View

Paoletti P, Neyton J . NMDA receptor subunits: function and pharmacology. Curr Opin Pharmacol. 2006; 7(1):39-47. DOI: 10.1016/j.coph.2006.08.011. View

Bakker S, Hoogendoorn M, Hendriks J, Verzijlbergen K, Caron S, Verduijn W . The PIP5K2A and RGS4 genes are differentially associated with deficit and non-deficit schizophrenia. Genes Brain Behav. 2007; 6(2):113-9. DOI: 10.1111/j.1601-183x.2006.00234.x. View

10.

Fan M, Raymond L . N-methyl-D-aspartate (NMDA) receptor function and excitotoxicity in Huntington's disease. Prog Neurobiol. 2006; 81(5-6):272-93. DOI: 10.1016/j.pneurobio.2006.11.003. View

11.

He Z, Li Z, Shi Y, Tang W, Huang K, Ma G . The PIP5K2A gene and schizophrenia in the Chinese population--a case-control study. Schizophr Res. 2007; 94(1-3):359-65. DOI: 10.1016/j.schres.2007.04.013. View

12.

Loonen A, van Praag H . Measuring movement disorders in antipsychotic drug trials: the need to define a new standard. J Clin Psychopharmacol. 2007; 27(5):423-30. DOI: 10.1097/jcp.0b013e31814f1105. View

13.

Estrada Sanchez A, Mejia-Toiber J, Massieu L . Excitotoxic neuronal death and the pathogenesis of Huntington's disease. Arch Med Res. 2008; 39(3):265-76. DOI: 10.1016/j.arcmed.2007.11.011. View

14.

Fedorenko O, Strutz-Seebohm N, Henrion U, Ureche O, Lang F, Seebohm G . A schizophrenia-linked mutation in PIP5K2A fails to activate neuronal M channels. Psychopharmacology (Berl). 2008; 199(1):47-54. DOI: 10.1007/s00213-008-1095-x. View

15.

Saggers-Gray L, Heriani H, Handoko H, Irmansyah I, Kusumawardhani A, Widyawati I . Association of PIP5K2A with schizophrenia: a study in an indonesian family sample. Am J Med Genet B Neuropsychiatr Genet. 2008; 147B(7):1310-3. DOI: 10.1002/ajmg.b.30736. View

16.

Al Hadithy A, Ivanova S, Pechlivanoglou P, Semke A, Fedorenko O, Kornetova E . Tardive dyskinesia and DRD3, HTR2A and HTR2C gene polymorphisms in Russian psychiatric inpatients from Siberia. Prog Neuropsychopharmacol Biol Psychiatry. 2009; 33(3):475-81. DOI: 10.1016/j.pnpbp.2009.01.010. View

17.

Fedorenko O, Tang C, Sopjani M, Foller M, Gehring E, Strutz-Seebohm N . PIP5K2A-dependent regulation of excitatory amino acid transporter EAAT3. Psychopharmacology (Berl). 2009; 206(3):429-35. DOI: 10.1007/s00213-009-1621-5. View

18.

van den Bout I, Divecha N . PIP5K-driven PtdIns(4,5)P2 synthesis: regulation and cellular functions. J Cell Sci. 2009; 122(Pt 21):3837-50. DOI: 10.1242/jcs.056127. View

19.

Al Hadithy A, Ivanova S, Pechlivanoglou P, Wilffert B, Semke A, Fedorenko O . Missense polymorphisms in three oxidative-stress enzymes (GSTP1, SOD2, and GPX1) and dyskinesias in Russian psychiatric inpatients from Siberia. Hum Psychopharmacol. 2009; 25(1):84-91. DOI: 10.1002/hup.1087. View

20.

Andreasen N, Pressler M, Nopoulos P, Miller D, Ho B . Antipsychotic dose equivalents and dose-years: a standardized method for comparing exposure to different drugs. Biol Psychiatry. 2009; 67(3):255-62. PMC: 3677042. DOI: 10.1016/j.biopsych.2009.08.040. View