PDF(Pubmed)
Abstract：
BACKGROUND: Developmental dyslexia, a complex neurodevelopmental disorder, not only affects children\'s academic performance but is also associated with increased healthcare costs, lower employment rates, and reduced productivity. The pathogenesis of dyslexia remains unclear and it is generally considered to be caused by the overlap of genetic and environmental factors. Systematically exploring the close relationship between exposure to environmental compounds and susceptibility genes in the development of dyslexia is currently lacking but high necessary.
METHODS: In this study, we systematically compiled 131 publicly reported susceptibility genes for dyslexia sourced from DisGeNET, OMIM, and GeneCards databases. Comparative Toxicogenomics Database database was used to explore the overlap between susceptibility genes and 95 environmental compounds, including metals, persistent organic pollutants, polycyclic aromatic hydrocarbons, and pesticides. Chemical bias towards the dyslexia risk genes was taken into account in the observation/expectation ratios > 1 and the corresponding P value obtained by hypergeometric probability test.
RESULTS: Our study found that the number of dyslexia risk genes targeted by each chemical varied from 1 to 109. A total of 35 chemicals were involved in chemical reactions with dyslexia-associated genes, with significant enrichment values (observed/expected dyslexia risk genes) ranging from 1.147 (Atrazine) to 66.901 (Dibenzo(a, h)pyrene).
CONCLUSIONS: The results indicated that dyslexia-associated genes were implicated in certain chemical reactions. However, these findings are exploratory, and further research involving animal or cellular experiments is needed.
METHODS: In this study, we systematically compiled 131 publicly reported susceptibility genes for dyslexia sourced from DisGeNET, OMIM, and GeneCards databases. Comparative Toxicogenomics Database database was used to explore the overlap between susceptibility genes and 95 environmental compounds, including metals, persistent organic pollutants, polycyclic aromatic hydrocarbons, and pesticides. Chemical bias towards the dyslexia risk genes was taken into account in the observation/expectation ratios > 1 and the corresponding P value obtained by hypergeometric probability test.
RESULTS: Our study found that the number of dyslexia risk genes targeted by each chemical varied from 1 to 109. A total of 35 chemicals were involved in chemical reactions with dyslexia-associated genes, with significant enrichment values (observed/expected dyslexia risk genes) ranging from 1.147 (Atrazine) to 66.901 (Dibenzo(a, h)pyrene).
CONCLUSIONS: The results indicated that dyslexia-associated genes were implicated in certain chemical reactions. However, these findings are exploratory, and further research involving animal or cellular experiments is needed.
摘要：
背景：发展性阅读障碍，一种复杂的神经发育障碍,不仅影响儿童的学习成绩，而且还与医疗费用的增加有关，就业率较低，降低了生产力。阅读障碍的发病机制尚不清楚，一般认为是由遗传和环境因素重叠引起的。目前缺乏系统地探索阅读障碍发展中环境化合物暴露与易感基因之间的密切关系，但很有必要。
方法：在本研究中，我们系统地汇编了131个公开报道的来自DisGeNet的阅读障碍易感基因，OMIM,和GeneCards数据库。比较毒性基因组学数据库数据库用于探索易感基因与95种环境化合物之间的重叠，包括金属,持久性有机污染物，多环芳烃，和杀虫剂。在观察/期望比>1和通过超几何概率检验获得的相应P值中，考虑了对阅读障碍风险基因的化学偏见。
结果：我们的研究发现，每种化学物质靶向的阅读障碍风险基因的数量从1到109不等。共有35种化学物质参与了与阅读障碍相关基因的化学反应，具有从1.147（阿特拉津）到66.901（二苯并（a，h)芘)。
结论：结果表明，阅读障碍相关基因与某些化学反应有关。然而,这些发现是探索性的，需要进一步研究涉及动物或细胞实验。
方法：在本研究中，我们系统地汇编了131个公开报道的来自DisGeNet的阅读障碍易感基因，OMIM,和GeneCards数据库。比较毒性基因组学数据库数据库用于探索易感基因与95种环境化合物之间的重叠，包括金属,持久性有机污染物，多环芳烃，和杀虫剂。在观察/期望比>1和通过超几何概率检验获得的相应P值中，考虑了对阅读障碍风险基因的化学偏见。
结果：我们的研究发现，每种化学物质靶向的阅读障碍风险基因的数量从1到109不等。共有35种化学物质参与了与阅读障碍相关基因的化学反应，具有从1.147（阿特拉津）到66.901（二苯并（a，h)芘)。
结论：结果表明，阅读障碍相关基因与某些化学反应有关。然而,这些发现是探索性的，需要进一步研究涉及动物或细胞实验。
