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在阿尔茨海默氏病模型中,TREM2脂质感应维持了微质反应

Yaming Wang¹, Marina Cella², Kaitlin Mallinson³

¹Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, USA.

|March 3, 2015

概括

在骨髓状细胞2 (TREM2) 上表达的触发受体 (TREM2) 缺乏,通过损害对粉样质斑块的微质反应,使阿尔茨海默病的病理状况恶化. R47H突变破坏了TREM2的脂质感应,突出显示了它在神经退行症中的作用.

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:

在骨髓细胞2 (TREM2) 上表达的触发受体是一个微质受体,与阿尔茨海默病 (AD) 风险有关.
一种罕见的R47H TREM2突变显著增加了AD易感性.

研究的目的:

在AD小鼠模型中研究TREM2缺乏和R47H突变的功能后果.
阐明TREM2在微质对粉样蛋白病理反应中的作用背后的分子机制.

主要方法:

利用AD的5XFAD小鼠模型来研究TREM2缺乏症和平缺乏症.
评估了微质集群,细胞亡以及对粉样β (Aβ) 斑块的反应.
研究了TREM2与与Aβ和神经元损伤相关的脂质配体的相互作用.

主要成果:

TREM2 缺陷和哈普洛缺陷加剧了Aβ积累.
缺乏TREM2的小鼠中的小质细胞无法在斑块周围聚集,并表现出增加的亡.
在受损的神经元上,TREM2感知到与Aβ相关的阳离子和离子脂质.
R47H突变会影响TREM2检测这些关键脂质连接体的能力.

结论:

在AD中,TREM2对于有效的微质对Aβ病理的反应至关重要.
由于TREM2的脂质感应受损,特别是R47H变体,导致AD的发病.
TREM2作为损伤相关脂质模式的传感器,调解微质神经保护功能.

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