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产前烟草暴露调节了遗传变异与儿童诊断 ADHD 及其症状领域的关联:一项基于社区的病例对照研究。

Prenatal Tobacco Exposure Modulated the Association of Genetic variants with Diagnosed ADHD and its symptom domain in children: A Community Based Case-Control Study.

机构信息

Department of Maternal and Child Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, P. R. China.

Department of Maternal, Child and Adolescent Health, School of Public Health, Lanzhou University, Lanzhou, Gansu, P. R. China.

出版信息

Sci Rep. 2019 Mar 12;9(1):4274. doi: 10.1038/s41598-019-40850-w.

DOI:10.1038/s41598-019-40850-w
PMID:30862909
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6414688/
Abstract

The purpose of our study was to test the hypothesis that prenatal tobacco smoking exposure (PSE) could modulate the association of genetic variants with ADHD. A community based case-control study was conducted among Chinese children and 168 ADHD patients and 233 controls were recruited by using combination diagnosis of DSM-IV, SNAP-IV and semi-structured clinical interview. Logistic regression analysis was performed to estimate the effect of prenatal tobacco smoking exposure and genotype frequencies on ADHD susceptibility individually by adjustment for potential confounders. Multiplicative and additive interaction analysis were performed to evaluate the interactions between risk genes and PSE with regard to ADHD. Prenatal tobacco smoke exposure was a significant risk factor of ADHD even after adjusted for other potential confounders. ADRA2A rs553668, DRD2 rs1124491 and SLC6A4 rs6354 were identified to be associated with ADHD. A significant multiplicative and additive gene-environment interactions were observed between the PSE and the ADRA2A rs553668 in relation to ADHD and ADHD-ODD. The risk of the genetic variants in ADHD was increased significantly if the child had prenatal tobacco exposure. The genetic risk for ADHD could be influenced by the presence of environmental risks. The environmental and the genetic risks are not distinct to each other. More gene-environment interaction studies were needed to reveal the etiology of ADHD.

摘要

我们的研究目的是验证这样一个假设,即产前吸烟暴露(PSE)可能会调节遗传变异与 ADHD 之间的关联。我们进行了一项基于社区的病例对照研究,在汉族儿童中招募了 168 名 ADHD 患者和 233 名对照。通过使用 DSM-IV、SNAP-IV 和半结构化临床访谈的联合诊断来进行。通过调整潜在的混杂因素,我们单独进行 logistic 回归分析来估计产前吸烟暴露和基因型频率对 ADHD 易感性的影响。我们进行了乘法和加法交互作用分析,以评估风险基因和 PSE 与 ADHD 之间的相互作用。即使在调整了其他潜在混杂因素后,产前吸烟暴露仍然是 ADHD 的一个显著危险因素。ADRA2A rs553668、DRD2 rs1124491 和 SLC6A4 rs6354 被鉴定与 ADHD 相关。在 ADHD 和 ADHD-ODD 方面,观察到 PSE 与 ADRA2A rs553668 之间存在显著的乘法和加法基因-环境交互作用。如果孩子有产前吸烟暴露,那么这些遗传变异在 ADHD 中的风险会显著增加。ADHD 的遗传风险可能会受到环境风险的影响。环境和遗传风险不是相互独立的。需要进行更多的基因-环境相互作用研究,以揭示 ADHD 的病因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a23e/6414688/f8093c964391/41598_2019_40850_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a23e/6414688/f8093c964391/41598_2019_40850_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a23e/6414688/f8093c964391/41598_2019_40850_Fig1_HTML.jpg

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