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在自闭症谱系障碍中对GABA/谷氨酸神经元分化的FOXG1依赖失调

Jessica Mariani¹, Gianfilippo Coppola¹, Ping Zhang²

¹Program in Neurodevelopment and Regeneration, Yale University, New Haven, CT 06520, USA; Child Study Center, Yale University, New Haven, CT 06520, USA.

|July 18, 2015

概括

研究人员使用大脑器官来研究自闭症谱系障碍 (ASD),发现称为FOXG1的基因导致特定神经元的过度产生,这可能解释了ASD的发展.

科学领域:

神经科学
发育生物学
遗传学

背景情况:

自闭症谱系障碍 (ASD) 是一种复杂的神经发育障碍,病理生理学不明.
研究自闭症需要复制人类大脑发育的模型,
异常性自闭症病例往往缺乏可识别的遗传原因,使病因研究复杂化.

研究的目的:

通过使用三维神经培养 (器官) 来研究严重的异常性自闭症神经发育变化.
在没有已知的基因组突变的情况下,确定ASD病理生理学的分子机制.

主要方法:

从患有严重特异性自闭症的个体的诱导多能干细胞 (iPSC) 生成三维神经器官.
转录组和基因网络分析以确定差异表达的基因和途径.
研究特定基因的功能作用,包括FOXG1.

主要成果:

由ASD衍生的器官显示细胞循环加速和GABAerg抑制神经元的过度产生.
观察到参与细胞增殖,神经元分化和突触组合的基因的升级.
转录因子FOXG1的过度表达被确定为GABAerg神经元过度产生的原因.
改变的基因网络表达和FOXG1水平与自闭症症状严重程度有正相关.

结论:

由FOXG1过度表达驱动的向GABAerg神经元命运的转变被认为是ASD的发育前体.
这些发现为特异性自闭症的病理生理学提供了洞察力.
来自iPSC的神经器官为研究神经发育障碍提供了有价值的模型.

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