Maternal exposure to bisphenol A may increase the risks of Parkinson's disease through down-regulation of fetal IGF-1 expression
Maternal exposure to bisphenol A may increase the risks of Parkinson's disease through down-regulation of fetal IGF-1 expression
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母亲接触双酚 A 可能会通过下调胎儿 IGF-1 表达而增加患帕金森病的风险
DOI：
10.1016/j.mehy.2013.10.023
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发表时间：
2014-03-01
影响因子：
4.7
通讯作者：
Liu, Jiayin
中科院分区：
文献类型：
--
作者：
Huang, Boxian;Jiang, Chunyan;Liu, Jiayin
迄今为止，帕金森病（PD）的发病机制仍不清楚。目前的研究暗示环境毒素可能是胎儿源性PD的潜在原因。双酚A（BPA）是广泛存在于环境中的雌激素类化合物。来自动物实验的重要证据表明，BPA干扰胎儿神经发育。结合以往的研究结果和我们对胚胎干细胞来源EB的研究，我们推测母亲在妊娠期暴露于低剂量BPA可能会降低IGF-1的表达，从而阻碍胎儿DA神经元的发育，最终增加PD的胎儿起源风险。我们的假设可能为PD的发病机制提供新的线索，并导致潜在的预防性治疗。皇冠版权所有（C）2013由爱思唯尔有限公司出版。保留所有权利。
So far, the pathogenesis of Parkinson's disease (PD) remains unclear. Current studies implicate environmental toxins may be potential causes of fetal origin of PD. BPA is a member of the family of estrogenic chemicals existing widely in environment. Significant evidences from animal experimentation have demonstrated that BPA interfere with fetal neurodevelopment. Based on previous reports and our research on EB derived from hESCs, we speculate that maternal exposure to low-dose BPA during gestational period may decrease IGF-1 expression, thus hinder the development of fetal DA neurons, and finally increase the risks of fetal origin of PD. Our hypothesis may shed new light on the pathogenesis of PD and lead to potential preventive treatments. Crown Copyright (C) 2013 Published by Elsevier Ltd. All rights reserved.