Genetics ignite focus on microglial inflammation in Alzheimer's disease.
Genetics ignite focus on microglial inflammation in Alzheimer's disease.
复制标题
DOI：
10.1186/s13024-015-0048-1
复制
发表时间：
2015-10-05
影响因子：
15.1
通讯作者：
Estus S
中科院分区：
文献类型：
--
作者：
Malik M;Parikh I;Vasquez JB;Smith C;Tai L;Bu G;LaDu MJ;Fardo DW;Rebeck GW;Estus S
在过去的五年里，一系列大规模的基因研究揭示了阿尔茨海默病(AD)的新危险因素。对这些危险因素的分析将注意力集中在免疫过程在AD中的作用，特别是小胶质细胞功能。在这篇综述中，我们讨论了对遗传学研究的解释。然后，我们重点关注与AD遗传学有关的六个影响小胶质细胞功能的基因：TREM2、CD33、CR1、ABCA7、SHIP1和APOE。我们回顾了有关这六种蛋白的生物学功能及其在AD发病机制中的推定作用的文献。然后，我们提出了一个模型，说明这些因素如何相互作用来调节AD的小胶质细胞功能。
In the past five years, a series of large-scale genetic studies have revealed novel risk factors for Alzheimer’s disease (AD). Analyses of these risk factors have focused attention upon the role of immune processes in AD, specifically microglial function. In this review, we discuss interpretation of genetic studies. We then focus upon six genes implicated by AD genetics that impact microglial function: TREM2, CD33, CR1, ABCA7, SHIP1, and APOE. We review the literature regarding the biological functions of these six proteins and their putative role in AD pathogenesis. We then present a model for how these factors may interact to modulate microglial function in AD.