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The effect of serotonin 1A receptor polymorphism on the cognitive function of premenstrual dysphoric disorder

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An Erratum to this article was published on 23 November 2013

Abstract

Estrogen and serotonin play vital roles in the mechanism of premenstrual dysphoric disorder (PMDD). Cognitive deficit in the premenstrual phase contributes to impaired life function among women with PMDD. The aim of this study was to evaluate the difficulties in cognitive control and working memory (WM) in PMDD and to explore the effects of gonadotropic hormone and polymorphism of serotonin 1A receptor (HTR1A; rs6295) on cognitive deficit in PMDD. Women with PMDD completed diagnostic interviewing, questionnaire assessment, the Go/Nogo task, 2-back and 3-back tasks, and gonadotropic hormone analysis in the premenstrual and follicular phases. Further, they were followed up for two menstrual cycles to confirm two consecutive symptomatic cycles. A total of 59 subjects with PMDD and 74 controls completed all evaluation, fulfilled the criteria, and entered into the final analysis. The results demonstrated cognitive control and WM decline in the premenstrual among women with PMDD. The G/G genotype of HTR1A (rs6295) was found to be associated with impaired WM in the premenstrual phase and premenstrual decline of cognitive function. It also contributed to the vulnerability of cognitive function to the menstrual cycle effect and PMDD effect. As the G/G genotype of HTR1A (rs6295) involves in reducing serotonin neurotransmission, our results provide insight into the serotonin mechanism of cognitive function among women with PMDD.

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Acknowledgments

This study was supported by grants from the National Science Council (NSC 100-2629-B-037 -001 -MY2) and the Kaohsiung Medical University Hospital (KMUH100-0R51).

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All other authors declare that they have no conflicts of interest.

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Correspondence to Chih-Hung Ko.

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Yen, JY., Tu, HP., Chen, CS. et al. The effect of serotonin 1A receptor polymorphism on the cognitive function of premenstrual dysphoric disorder. Eur Arch Psychiatry Clin Neurosci 264, 729–739 (2014). https://doi.org/10.1007/s00406-013-0466-4

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  • DOI: https://doi.org/10.1007/s00406-013-0466-4

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