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.
| Original language | English |
|---|---|
| Pages (from-to) | 1-6 |
| Number of pages | 6 |
| Journal | International Journal of Neuropsychopharmacology |
| Volume | 18 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 1 Jan 2015 |
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Keywords
- gene polymorphism
- medium spiny neurons
- neurotoxicity
- PIP5K2A
- schizophrenia
- tardive dyskinesia
ASJC Scopus subject areas
- Pharmacology
- Psychiatry and Mental health
- Pharmacology (medical)
Cite this
Association study indicates a protective role of phosphatidylinositol-4-phosphate-5-kinase against tardive dyskinesia. / Fedorenko, Olga Yu; Loonen, Anton J.M.; Lang, Florian; Toshchakova, Valentina A.; Boyarko, Evgenia G.; Semke, Arkadiy V.; Bokhan, Nikolay A.; Govorin, Nikolay V.; Aftanas, Lyubomir I.; Ivanova, Svetlana A.
In: International Journal of Neuropsychopharmacology, Vol. 18, No. 6, 01.01.2015, p. 1-6.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Association study indicates a protective role of phosphatidylinositol-4-phosphate-5-kinase against tardive dyskinesia
AU - Fedorenko, Olga Yu
AU - Loonen, Anton J.M.
AU - Lang, Florian
AU - Toshchakova, Valentina A.
AU - Boyarko, Evgenia G.
AU - Semke, Arkadiy V.
AU - Bokhan, Nikolay A.
AU - Govorin, Nikolay V.
AU - Aftanas, Lyubomir I.
AU - Ivanova, Svetlana A.
PY - 2015/1/1
Y1 - 2015/1/1
N2 - 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.
AB - 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.
KW - gene polymorphism
KW - medium spiny neurons
KW - neurotoxicity
KW - PIP5K2A
KW - schizophrenia
KW - tardive dyskinesia
UR - http://www.scopus.com/inward/record.url?scp=84939192245&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84939192245&partnerID=8YFLogxK
U2 - 10.1093/ijnp/pyu098
DO - 10.1093/ijnp/pyu098
M3 - Article
VL - 18
SP - 1
EP - 6
JO - International Journal of Neuropsychopharmacology
JF - International Journal of Neuropsychopharmacology
SN - 1461-1457
IS - 6
ER -