Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5811822 | Medical Hypotheses | 2014 | 5 Pages |
Abstract
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.
Keywords
NHANESOct4ICMhomeoboxIGF-1RIRS-1NANOGSOX17ESCsMedulla oblongataDOPACMPTPIGF-1qRT-PCRhESCsEDCBPA6-OHDAHoxa1FACSPOU class 5 homeobox 1HOXneural cell adhesion molecule 1NCAM1SNpcAmygdalaStage-specific embryonic antigen-4AktAMYInsulin like growth factor-1MEDNational Health and Nutrition Examination SurveyWinglessBisphenol AParkinson’s diseaseAFPInner cell massembryoid bodyEnvironmental endocrine disruptorsDopaminedihydroxyphenylacetic acidinsulin receptor substrate 1human embryonic stem cellsEmbryonic stem cellsfluorescence activated cell sortingSubstantia nigra compactaHIPfollicle-stimulating hormoneFSHHippocampusquantitative real time polymerase chain reactionprotein kinase Binsulin-like growth factor 1 receptor
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Authors
Boxian Huang, Chunyan Jiang, Jian Luo, Yugui Cui, Lianju Qin, Jiayin Liu,