Department of Maternal and Child Health and MOE (Ministry of Education) Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Maternal and Child Health and MOE (Ministry of Education) Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Neurotoxicology. 2022 Sep;92:102-109. doi: 10.1016/j.neuro.2022.08.004. Epub 2022 Aug 5.
Excessive exposure to manganese is harmful for neurodevelopment, causing intellectual disability, decreased cognitive ability and diminished language quotients. However, little is known about the link between manganese, genetic susceptibility and the risk of dyslexia. We aim to examine the association between manganese exposure and dyslexia and to test whether the SLC6A3 gene would modify this relationship.
A case-control study was conducted among 239 dyslexic children and 230 controls in China. Urinary manganese concentrations were assessed by inductively coupled plasma mass spectrometry (ICP-MS). Two single nucleotide polymorphisms (rs2975226 and rs27072) in the SLC6A3 gene were selected.
The rs2975226 polymorphism was associated with dyslexia within the recessive model (OR = 1.74, 95 % CI = 1.06-2.86) and the additive model (OR = 1.69, 95 % CI = 1.10-2.61) after multivariate adjustment. Modification effects on the relationship of manganese levels in urine with the risk of dyslexia were suggested in rs27072 (P-value for interaction = 0.003). Furthermore, the highest quartile of urinary manganese was found to have a 3.87-fold (95 % CI = 1.39-10.74) elevated dyslexia risk compared with the lowest quartile among the rs27072 mutation carriers.
The rs2975226 polymorphism was associated with dyslexia and manganese exposure could interact with the rs27072 mutation to increase the risk of dyslexia.
过量接触锰对神经发育有害，可导致智力障碍、认知能力下降和语言商数降低。然而，人们对锰、遗传易感性与阅读障碍风险之间的联系知之甚少。我们旨在研究锰暴露与阅读障碍之间的关联，并检验 SLC6A3 基因是否会改变这种关系。
在中国进行了一项病例对照研究，纳入了 239 名阅读障碍儿童和 230 名对照。采用电感耦合等离子体质谱法（ICP-MS）检测尿锰浓度。选择 SLC6A3 基因中的两个单核苷酸多态性（rs2975226 和 rs27072）。
rs2975226 多态性与多变量调整后的隐性模型（OR=1.74，95%CI=1.06-2.86）和加性模型（OR=1.69，95%CI=1.10-2.61）中的阅读障碍相关。rs27072 提示对尿锰水平与阅读障碍风险关系的修饰作用（交互作用 P 值=0.003）。此外，与最低四分位数相比，rs27072 突变携带者的尿锰最高四分位数发生阅读障碍的风险增加了 3.87 倍（95%CI=1.39-10.74）。
rs2975226 多态性与阅读障碍相关，且锰暴露可能与 rs27072 突变相互作用，增加阅读障碍的风险。
