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功能性脑源性神经营养因子和多巴胺受体 D2/多巴胺受体 D3 基因变异的相互作用与健康人群的述情障碍有关。

Interaction effect of functional variants of the BDNF and DRD2/ANKK1 gene is associated with alexithymia in healthy human subjects.

机构信息

Department of Psychology, University of Bonn, Kaiser-Karl-Ring 9, Bonn, Germany.

出版信息

Psychosom Med. 2011 Jan;73(1):23-8. doi: 10.1097/PSY.0b013e31820037c1. Epub 2010 Nov 19.

DOI:10.1097/PSY.0b013e31820037c1
PMID:21097659
Abstract

OBJECTIVE

To test the hypothesis that the interaction between the brain-derived neurotrophic factor (BDNF) and dopamine receptor D(2) (DRD2)/ANKK1 gene contributes to individual differences in alexithymia. The personality construct of alexithymia refers to difficulties in emotional self-regulation and contributes as a risk factor to several mental disorders. Alexithymic individuals show an impoverished conscious experience of emotions but an intact autonomic emotional response. Persons with high alexithymia scores reportedly show a reduced activation of the anterior cingulate cortex (ACC) during the processing of emotional stimuli. An interaction between two polymorphisms on the BDNF and DRD2/ANKK1 gene has been recently associated with reduced gray matter volume in the ACC and higher trait anxiety.

METHODS

We conducted a genetic association study. A total of 664 healthy participants completed the Toronto Alexithymia Scale questionnaire and were genotyped for the BDNF Val66Met (rs6265) and the DRD2/ANKK1 Taq IA (rs1800497) polymorphisms.

RESULTS

Carriers of at least one BDNF 66Met and one DRD2/ANKK1 A1 allele showed the highest scores in the total Toronto Alexithymia Scale and in the subscale "Difficulties Identifying Feelings."

CONCLUSION

In line with recent studies investigating the role of BDNF Val66Met and DRD2/ANKK1 Taq IA polymorphisms on anxiety and gray matter volume in the ACC, our findings provide the first evidence for a genetic contribution to alexithymia.

摘要

目的

检验脑源性神经营养因子(BDNF)与多巴胺受体 D2(DRD2)/ANKK1 基因相互作用是否会导致述情障碍的个体差异。述情障碍的人格结构是指情绪自我调节的困难,它是几种精神障碍的危险因素。述情障碍个体表现出情绪意识体验的匮乏,但自主情绪反应完好。据报道,高述情障碍评分者在处理情绪刺激时,前扣带皮层(ACC)的激活减少。BDNF 和 DRD2/ANKK1 基因的两个多态性之间的相互作用最近与 ACC 中灰质体积减少和特质焦虑增加有关。

方法

我们进行了一项遗传关联研究。共有 664 名健康参与者完成了多伦多述情障碍量表问卷,并对 BDNF Val66Met(rs6265)和 DRD2/ANKK1 TaqIA(rs1800497)多态性进行了基因分型。

结果

至少携带一个 BDNF 66Met 和一个 DRD2/ANKK1 A1 等位基因的携带者在多伦多述情障碍量表总分和“识别困难”分量表中得分最高。

结论

与最近研究 BDNF Val66Met 和 DRD2/ANKK1 TaqIA 多态性对 ACC 中的焦虑和灰质体积的作用一致,我们的发现为述情障碍的遗传贡献提供了第一个证据。

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