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使用突变tau器官模拟神经退行

Laura Pellegrini¹, Madeline A Lancaster¹

¹MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.

|August 20, 2021

概括

研究人员开发了脑器官来研究前性痴呆症 (FTD). 这些器官显示出异常的拼接和谷氨酸信号作为MAPT相关FTD发病的关键早期事件.

科学领域:

神经科学
遗传学
细胞生物学

背景情况:

像前性痴呆症 (FTD) 这样的神经退行性疾病需要更好地了解早期的病原性事件.
微管相关蛋白tau (MAPT) 基因的突变与FTD有关.
开发有效的预防和治疗策略需要更深入地了解疾病的开始.

研究的目的:

研究前性痴呆 (FTD) 发病的早期分子和细胞事件.
探索微管相关蛋白tau (MAPT) 突变在疾病发病中的作用.
确定导致FTD神经退行的新机制.

主要方法:

从患者特异性诱导多能干细胞 (iPSC) 获得的人类大脑器官的生成和利用.
在有机体模型中分析基因表达,拼接模式和细胞信号通路.
研究MAPT突变对神经元发育和功能的功能影响.

主要成果:

携带MAPT突变的大脑器官回顾了FTD病理的关键方面.
异常RNA拼接事件被确定为MAPT突变的早期后果.
在受影响的器官中观察到谷氨酸信号通路的失调.

结论:

在MAPT相关的FTD中,早期的致病性事件涉及异常拼接和改变的谷氨酸信号.
大脑器官为研究FTD病变提供了有价值的平台.
这些发现为旨在预防或治疗FTD的治疗干预提供了新的目标.

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