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    請使用永久網址來引用或連結此文件: https://tkuir.lib.tku.edu.tw/dspace/handle/987654321/58783

    題名: RGS4 Polymorphisms Predict Clinical Manifestations and Responses to Risperidone Treatment in Patients With Schizophrenia
    作者: Lane, Hsien-Yuan;Liu, Yi-Ching;Huang, Chieh-Liang;Chang, Yue-Cune;Wu, Po-Lun;Huang, Chiung-Hsien;Tasi, Guochuan E.
    貢獻者: 淡江大學數學學系
    日期: 2008-02
    上傳時間: 2011-10-01 21:10:53 (UTC+8)
    出版者: Philadelphia: Lippincott Williams & Wilkins
    摘要: Objective: Polymorphisms of the gene encoding the regulator of G-protein signaling subtype 4 (RGS4) are associated with schizophrenia. This study aims to investigate the association of 4 RGS4 polymorphisms (single nucleotide polymorphisms [SNPs] 1, 4, 7, and 18), implicated in previous studies, with baseline symptoms and treatment response to risperidone in patients with schizophrenia.
    Methods: One hundred twenty patients with acutely exacerbated schizophrenia who had never been treated by atypical antipsychotics were recruited. They received optimal treatment of risperidone for up to 42 days in the inpatient research unit. Patients' social functions were monitored by Nurses' Observation Scale for Inpatients Evaluation and clinical manifestations, by Positive and Negative Syndrome Scale.
    Results: At baseline status, the A/A genotype at SNP7 of RGS4 was associated with poorer social function when compared with the G/G genotype. After risperidone treatment, the A/A genotype at SNP1 was associated with greater improvement at social function, and the A/A genotype at SNP18 was associated with greater improvement at social function, Positive and Negative Syndrome Scale total score, and positive- and negative-symptom subscale.
    Conclusions: These findings suggest that RGS4 variances influence clinical manifestations of schizophrenia as well as the treatment response to risperidone, suggesting that RGS4 plays a role in the fundamental process of disease pathophysiology.
    關聯: Journal of Clinical Psychopharmacology 28(1), pp.64-68
    DOI: 10.1097/jcp.0b013e3181603f5a
    顯示於類別:[數學學系暨研究所] 期刊論文


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