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The presence of both serotonin 1A receptor (HTR1A) and dopamine transporter (DAT1) gene variants increase the risk of borderline personality disorder

机译:血清素1A受体(HTR1A)和多巴胺转运蛋白(DAT1)基因变体的存在增加了边缘型人格障碍的风险

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摘要

Dysfunction in the dopaminergic and serotonergic neurotransmitter systems has been demonstrated to be important in the etiology of borderline personality disorder (BPD). We investigated the relationship of two BPD risk factors, the HTR1A promoter polymorphism -1019C > G (rs6295) and the dopamine transporter (DAT1) repeat allele, with BPD in a major depressive disorder cohort of 367 patients. Out-patients with major depressive disorder were recruited for two treatment trials and assessed for personality disorders, including BPD. DNA samples were collected and the rs6295 polymorphism was detected with a TaqMan® assay. The DAT1 repeat allele was genotyped using a modified PCR method. The impact of polymorphisms on BPD was statistically analyzed using uncontrolled logistic and multiple logistic regression models. BPD patients had higher frequencies of the DAT1 9,9 (OR = 2.67) and 9,10 (OR = 3.67) genotypes and also those homozygous HTR1A G allele (OR = 2.03). No significant interactions between HTR1A and DAT1 genotypes, were observed; however, an increased risk of BPD was observed for those patients who were either 9,10; G,G (OR = 6.64) and 9,9; C,G (OR = 5.42). Furthermore, the odds of BPD in patients exhibiting high-risk variants of these two genes differed from those of patients in low-risk groups by up to a factor of 9. Our study provides evidence implicating the importance of the serotonergic and dopaminergic systems in BPD and that the interaction between genes from different neurotransmitters may play a role in the susceptibility to BPD.
机译:多巴胺能和5-羟色胺能神经递质系统功能障碍已被证明在边缘性人格障碍(BPD)的病因中很重要。我们调查了两个BPD危险因素之间的关系,即HTR1A启动子多态性-1019C> G(rs6295)和多巴胺转运蛋白(DAT1)重复等位基因与BPD在367名患者的主要抑郁症队列中的关系。招募患有重度抑郁症的门诊患者进行两项治疗试验,并评估其人格障碍,包括BPD。收集DNA样品,并用TaqMan ®分析检测rs6295多态性。使用改良的PCR方法对DAT1重复等位基因进行基因分型。使用不受控制的逻辑模型和多逻辑回归模型对多态性对BPD的影响进行了统计分析。 BPD患者的DAT1 9,9(OR = 2.67)和9,10(OR = 3.67)基因型以及纯合HTR1A G等位基因(OR = 2.03)的频率更高。没有观察到HTR1A和DAT1基因型之间的显着相互作用。然而,对于那些9,10的患者,观察到BPD的风险增加。 G,G(OR = 6.64)和9,9; C,G(OR = 5.42)。此外,表现出这两个基因的高风险变异的患者中BPD的几率与低风险人群的差异高达9。我们的研究提供了证据,表明BPD中血清素能和多巴胺能系统的重要性以及来自不同神经递质的基因之间的相互作用可能在对BPD的易感性中起作用。

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