Rivest Serge
Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Blvd., Québec, Canada.
Cell Res. 2015 May;25(5):535-6. doi: 10.1038/cr.2015.37. Epub 2015 Mar 31.
In a recent paper published in Cell, Wang et al. report that deficiency of triggering receptor expressed on myeloid cells 2 (TREM2) augments amyloid β accumulation and neuronal loss in a mouse model of Alzheimer's disease. TREM2 acts as a signaling receptor involved in innate immunity for the natural clearance of this toxic protein by microglia.
在最近发表于《细胞》杂志的一篇论文中,王等人报告称,在阿尔茨海默病小鼠模型中,髓样细胞2(TREM2)上表达的触发受体缺乏会加剧淀粉样β蛋白的积累和神经元损失。TREM2作为一种信号受体,参与先天免疫,由小胶质细胞对这种有毒蛋白质进行自然清除。