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携带TREM2 R47H/+突变的iPSC衍生微质具有促炎作用,并促进突触损失

Jay Penney^1,2,3, William T Ralvenius^1,2, Anjanet Loon^1,2

¹Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

|November 16, 2023

概括

TREM2 R47H/+突变会损害微质功能,影响细胞过程和炎症反应. 微质中的这种功能障碍可能会导致阿尔茨海默氏症的发展.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
遗传学是一个遗传学.

背景情况:

微质在像阿尔茨海默氏症 (AD) 这样的神经退行性疾病中起着至关重要的作用.
TREM2基因的突变,特别是R47H/+,与AD风险增加有关.

研究的目的:

研究人类微质中TREM2 R47H/+突变的功能后果.
阐明TREM2 R47H/+对AD病理学的分子机制.

主要方法:

利用基因编辑和人类诱导的多能干细胞衍生微质细胞模型.
在神经元-微细胞共同培养中开发了体外激光诱导的损伤模型.
分析了小鼠大脑中的转录变化,细胞功能和突触密度.

主要成果:

TREM2 R47H/+微质表现出改变的基因表达,具有促炎特征.
观察到微质运动受损,基质吸收和对炎症刺激的过度反应.
TREM2 R47H/+微质细胞对损伤的反应受损,并与体内突触密度降低有关.

结论:

TREM2 R47H/+突变对微质基因表达和功能产生不利影响.
这些功能缺陷,包括不适当的突触修剪,可能导致阿尔茨海默病的风险增加.

关键词:

阿尔茨海默病的疾病阿尔茨海默病的疾病.诱导多能干细胞的诱导干细胞.这是一种炎症炎症炎症炎症.微质细胞中的微质细胞神经退行症的神经退行症在骨髓细胞2 (TREM2) 上表达的触发受体 (TREM2)

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