Association between Tardive Dyskinesia and T103C Polymorphisms of 5-HT2A Receptor Gene
Journal of the Korean Society of Biological Psychiatry
;
: 133-140, 2003.
Artigo
em Coreano
| WPRIM
| ID: wpr-724831
ABSTRACT
OBJECTIVE:
Some candidate gene polymorphisms were reported to be associated with tardive dyskinesia (TD). The aim of this study was to investigate the association of the 5-HT2A receptor gene polymorphisms with TD in Korean schizophrenic subjects.METHOD:
Subjects were of 59 schizophrenic patients with TD and 60 schizophrenic patients without TD for studying of 5-HT2A receptor gene polymorphisms. TD was evaluated using the Abnormal Involuntary Movement Scale(AIMS). Genomic DNA was amplified by PCR and digestion with MspI and BsmI.RESULT:
There were no statistically significant differences in the demographic variables, such as age, male to female percentage, duration of illnesses and duration of antipsychotic drug exposure between the TD group and control group. 1) T102C polymorphisms and TD Comparing the TD group and control group, the 102T/C allele was associated with a significantly increased risk for TD (chi2=5.560, df=1, p=0.018). 2) Three AIMS categories of TD and T102C genotype. There were statistically significant differences in the three AIMS categories(chi2=6.835, df=2, p=0.033).CONCLUSION:
These result suggest 102T/C genotypes of the 5-HT2A receptor gene are related to the development of TD. The 102T/C genotypes were associated with significantly higher AIMS orofacial dyskinesia scores. These findings suggest that the 5-HT2A receptor gene is significantly associated with susceptibility to TD in patients with chronic schizophrenia.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Esquizofrenia
/
DNA
/
Reação em Cadeia da Polimerase
/
Discinesias
/
Receptor 5-HT2A de Serotonina
/
Digestão
/
Alelos
/
Genótipo
/
Transtornos dos Movimentos
Limite:
Feminino
/
Humanos
/
Masculino
Idioma:
Coreano
Revista:
Journal of the Korean Society of Biological Psychiatry
Ano de publicação:
2003
Tipo de documento:
Artigo
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