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血清素转运体基因启动子多态性(5HTTLPR)与有或无抑郁症家族史的健康女性色氨酸耗竭行为反应之间的关联。

Association between serotonin transporter gene promoter polymorphism (5HTTLPR) and behavioral responses to tryptophan depletion in healthy women with and without family history of depression.

作者信息

Neumeister Alexander, Konstantinidis Anastasios, Stastny Juergen, Schwarz Markus J, Vitouch Oliver, Willeit Matthaus, Praschak-Rieder Nicole, Zach Johanna, de Zwaan Martina, Bondy Brigitta, Ackenheil Manfred, Kasper Siegfried

机构信息

National Institutes of Health, NIMH, Mood and Anxiety Disorders Program, Bethesda, MD 20892-2670.

出版信息

Arch Gen Psychiatry. 2002 Jul;59(7):613-20. doi: 10.1001/archpsyc.59.7.613.

Abstract

BACKGROUND

Evidence suggests that serotonin transporter gene promoter polymorphism (5HTTLPR)-dependent low transcriptional activity of the human serotonin transporter gene may be a genetic susceptibility factor for depression. We studied the behavioral responses to tryptophan depletion (TD) in healthy women with and without a first-degree family history of depression and examined the relationship to 5HTTLPR alleles.

METHODS

Twenty-four healthy women with a negative family history of depression and 21 women with a positive family history of depression were genotyped for the polymorphism of the 5HTTLPR and then entered a double-blind, placebo-controlled, randomized crossover TD study. The effects of these interventions were assessed with measures of depression and plasma tryptophan levels.

RESULTS

The TD induced a robust decrease of plasma tryptophan levels in all women irrespective of family history of depression or 5HTTLPR genotypes. The s/s genotype of the 5HTTLPR was associated with an increased risk of developing depressive symptoms during TD irrespective of family history. In contrast, individuals with the l/l genotype did not develop depressive symptoms, irrespective of family history. Finally, s/l subjects without family history showed a mood response that was intermediate between the s/s and l/l subjects, while s/l subjects with a family history of depression showed the same depressiogenic effect of TD as seen in the s/s subjects.

CONCLUSIONS

The results of the present study suggest that the s-allele of the 5HTTLPR and a positive family history of depression are additive risk factors for the development of depression during TD.

摘要

背景

有证据表明,人类血清素转运体基因启动子多态性(5HTTLPR)依赖的低转录活性可能是抑郁症的一个遗传易感性因素。我们研究了有或无抑郁症一级家族史的健康女性对色氨酸耗竭(TD)的行为反应,并探讨了其与5HTTLPR等位基因的关系。

方法

对24名抑郁症家族史阴性的健康女性和21名抑郁症家族史阳性的女性进行5HTTLPR多态性基因分型,然后进入一项双盲、安慰剂对照、随机交叉TD研究。通过抑郁量表和血浆色氨酸水平评估这些干预措施的效果。

结果

无论抑郁症家族史或5HTTLPR基因型如何,TD均导致所有女性血浆色氨酸水平显著下降。5HTTLPR的s/s基因型与TD期间出现抑郁症状的风险增加相关,与家族史无关。相比之下,无论家族史如何,l/l基因型的个体均未出现抑郁症状。最后,无家族史的s/l受试者的情绪反应介于s/s和l/l受试者之间,而有抑郁症家族史的s/l受试者表现出与s/s受试者相同的TD致抑郁作用。

结论

本研究结果表明,5HTTLPR的s等位基因和抑郁症阳性家族史是TD期间抑郁症发生的累加风险因素。

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