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产前性激素暴露与自闭症谱系障碍的发展有关。

Prenatal Sex Hormone Exposure Is Associated with the Development of Autism Spectrum Disorder.

机构信息

Department of Neuroscience and Cell Biology, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan.

United Graduate School of Child Development, Osaka University, Suita 565-0871, Japan.

出版信息

Int J Mol Sci. 2023 Jan 22;24(3):2203. doi: 10.3390/ijms24032203.

DOI:10.3390/ijms24032203
PMID:36768521
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9916422/
Abstract

Sexual differentiation is a major developmental process. Sex differences resulting from sexual differentiation have attracted the attention of researchers. Unraveling what contributes to and underlies sex differences will provide valuable insights into the development of neurodevelopmental disorders that exhibit sex biases. Autism spectrum disorder (ASD) is a neurodevelopmental disorder that affects an individual's social interaction and communication abilities, and its male preponderance has been consistently reported in clinical studies. The etiology of male preponderance remains unclear, but progress has been made in studying prenatal sex hormone exposure. The present review examined studies that focused on the association between prenatal testosterone exposure and ASD development, as well as sex-specific behaviors in individuals with ASD. This review also included studies on maternal immune activation-induced developmental abnormalities that also showed striking sex differences in offspring and discussed its possible interacting roles in ASD so as to present a potential approach for future studies on sex biases in ASD.

摘要

性分化是一个主要的发育过程。性分化产生的性别差异引起了研究人员的关注。揭示导致性别差异的因素及其基础将为神经发育障碍的发展提供有价值的见解,这些障碍表现出性别偏见。自闭症谱系障碍(ASD)是一种神经发育障碍,影响个体的社交互动和沟通能力,其男性优势在临床研究中一直有报道。男性优势的病因仍不清楚,但在研究产前性激素暴露方面已经取得了进展。本综述检查了专注于产前睾酮暴露与 ASD 发展之间关系以及 ASD 个体中性别特异性行为的研究。本综述还包括关于母体免疫激活诱导的发育异常的研究,这些研究也显示了后代明显的性别差异,并讨论了其在 ASD 中可能的相互作用角色,以期为 ASD 中性别偏见的未来研究提供一种潜在的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1daf/9916422/0110b6c046aa/ijms-24-02203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1daf/9916422/726afc425449/ijms-24-02203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1daf/9916422/ab99eff648a9/ijms-24-02203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1daf/9916422/0110b6c046aa/ijms-24-02203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1daf/9916422/726afc425449/ijms-24-02203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1daf/9916422/ab99eff648a9/ijms-24-02203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1daf/9916422/0110b6c046aa/ijms-24-02203-g003.jpg

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