Tanner Samuel, Thomson Sarah, Drummond Katherine, O'Hely Martin, Symeonides Christos, Mansell Toby, Saffery Richard, Sly Peter D, Collier Fiona, Burgner David, Sugeng Eva J, Dwyer Terence, Vuillermin Peter, Ponsonby Anne-Louise
Developing Brain Division, The Florey Institute for Neuroscience and Mental Health, Parkville, VIC 3052, Australia.
Murdoch Children's Research Institute, Royal Children's Hospital, University of Melbourne, Parkville, VIC 3052, Australia.
Antioxidants (Basel). 2022 Mar 29;11(4):659. doi: 10.3390/antiox11040659.
The developing brain is highly sensitive to environmental disturbances, and adverse exposures can act through oxidative stress. Given that oxidative stress susceptibility is determined partly by genetics, multiple studies have employed genetic scores to explore the role of oxidative stress in human disease. However, traditional approaches to genetic score construction face a range of challenges, including a lack of interpretability, bias towards the disease outcome, and often overfitting to the study they were derived on. Here, we develop an alternative strategy by first generating a genetic pathway function score for oxidative stress (gPFSox) based on the transcriptional activity levels of the oxidative stress response pathway in brain and other tissue types. Then, in the Barwon Infant Study (BIS), a population-based birth cohort (n = 1074), we show that a high gPFSox, indicating reduced ability to counter oxidative stress, is linked to higher autism spectrum disorder risk and higher parent-reported autistic traits at age 4 years, with AOR values (per 2 additional pro-oxidant alleles) of 2.10 (95% CI (1.12, 4.11); p = 0.024) and 1.42 (95% CI (1.02, 2.01); p = 0.041), respectively. Past work in BIS has reported higher prenatal phthalate exposure at 36 weeks of gestation associated with offspring autism spectrum disorder. In this study, we examine combined effects and show a consistent pattern of increased neurodevelopmental problems for individuals with both a high gPFSox and high prenatal phthalate exposure across a range of outcomes, including high gPFSox and high DEHP levels against autism spectrum disorder (attributable proportion due to interaction 0.89; 95% CI (0.62, 1.16); p < 0.0001). The results highlight the utility of this novel functional genetic score and add to the growing evidence implicating gestational phthalate exposure in adverse neurodevelopment.
发育中的大脑对环境干扰高度敏感,不良暴露可通过氧化应激起作用。鉴于氧化应激易感性部分由遗传决定,多项研究采用基因评分来探究氧化应激在人类疾病中的作用。然而,传统的基因评分构建方法面临一系列挑战,包括缺乏可解释性、对疾病结局有偏向性,且常常过度拟合其来源的研究。在此,我们开发了一种替代策略,首先基于大脑和其他组织类型中氧化应激反应途径的转录活性水平生成氧化应激的基因途径功能评分(gPFSox)。然后,在基于人群的出生队列巴旺婴儿研究(BIS,n = 1074)中,我们发现高gPFSox表明对抗氧化应激的能力降低,与4岁时更高的自闭症谱系障碍风险和更高的父母报告的自闭症特征相关,AOR值(每增加2个促氧化等位基因)分别为2.10(95%CI(1.12,4.11);p = 0.024)和1.42(95%CI(1.02,2.01);p = 0.041)。BIS过去的研究报告称,妊娠36周时产前邻苯二甲酸盐暴露较高与后代自闭症谱系障碍有关。在本研究中,我们研究了联合效应,结果表明,对于gPFSox高且产前邻苯二甲酸盐暴露高的个体,在一系列结局中存在神经发育问题增加的一致模式,包括高gPFSox和高DEHP水平与自闭症谱系障碍的关系(交互作用导致的归因比例为0.89;95%CI(0.62,1.16);p < 0.0001)。这些结果突出了这种新型功能基因评分的实用性,并进一步证明了妊娠期间邻苯二甲酸盐暴露与不良神经发育有关的证据越来越多。