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首页> 外文期刊>Pharmacogenetics and genomics >A splice site polymorphism in the G-protein beta subunit influences antidepressant efficacy in depression.
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A splice site polymorphism in the G-protein beta subunit influences antidepressant efficacy in depression.

机译：G蛋白β亚基的剪接位点多态性影响抑郁症的抗抑郁功效。

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OBJECTIVE: Recent evidence suggests that signalling cascades located downstream of monoamine receptors are altered following antidepressant treatment. Our objective was to investigate whether genetic polymorphisms in genes involved in these signalling cascades influenced antidepressant efficacy. METHODS: Polymorphisms in the G-protein beta subunit GNB3, the cAMP response element binding protein 1 gene (CREB1), the brain derived neurotrophic factor (BDNF) and CREB binding protein (CREBBP) were studied in well characterised unipolar (n=166) and early onset (n=102) depressive populations and correlated with treatment response. RESULTS: The GNB3 C825T polymorphism, which results in a 41 amino acid deletion, was significantly associated with lack of remission (OR=0.18, P=0.02) and lack of response (OR=0.26, P=0.03) following 2nd switch treatment. A cytosine deletion 16 base pairs from the start of exon 8 in CREB1 was found more frequently in remitters and responders to 2nd switch antidepressant drug therapy, although these differences failed to reach significance. Polymorphisms detected BDNF (G196A) and CREBBP (T651 C) did not appear to influence antidepressant response. CONCLUSIONS: These results suggest that inheritance of the GNB3C825T allele may significantly influence antidepressant response and emphasises the potential importance of polymorphisms in genes in signalling cascades activated by commonly prescribed antidepressants.
机译：目的：最近的证据表明，抗抑郁药治疗后单胺受体下游的信号级联反应发生了改变。我们的目的是调查参与这些信号级联反应的基因中的遗传多态性是否影响抗抑郁药的疗效。方法：在特征明确的单极（n = 166）中研究了G蛋白β亚基GNB3，cAMP反应元件结合蛋白1基因（CREB1），脑源性神经营养因子（BDNF）和CREB结合蛋白（CREBBP）的多态性。和早期发作（n = 102）的抑郁症人群，并与治疗反应相关。结果：GNB3 C825T多态性导致41个氨基酸缺失，与第二次转换治疗后缓解缺乏（OR = 0.18，P = 0.02）和反应缺乏（OR = 0.26，P = 0.03）显着相关。在CREB1外显子8起始处的胞嘧啶缺失16个碱基对在第二次转换抗抑郁药物治疗的缓解者和应答者中更为常见，尽管这些差异未能达到显着性。检测到的BDNF（G196A）和CREBBP（T651 C）的多态性似乎并未影响抗抑郁药的反应。结论：这些结果表明，GNB3C825T等位基因的遗传可能显着影响抗抑郁反应，并强调了基因多态性在通常被规定的抗抑郁药激活的信号级联反应中的潜在重要性。

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