摘要
阿尔茨海默氏病（AD）是一种与年龄相关的神经退行性疾病，被逐渐下降的认知能力下降所识别，具有严重的个人和社会经济意义。最近，已经确定了一些AD的遗传因素，引起了AD生物学不同领域的研究人员的广泛关注以及可能的新治疗靶标。在髓样细胞2（TREM2）基因上表达的触发受体的其他形式是此类风险因素的示例，这些风险因素会增加患上AD的风险。理解TREM2的功能保证可以深入了解神经炎症如何促进AD病理。小胶质细胞TREM2缺乏到增加tau病理学与激活神经元应激激酶的频繁增强相结合。通过这些发现清楚地证明了TREM2参与中枢神经系统的tau相关的先天免疫应答的调节。然而，TREM2的降低水平是否通过改变tau的清除率和病理升级或通过小胶质细胞与神经元之间的直接接触来辅助tau病理，并且需要研究任何其他可能的机制。这篇综述简要总结了TREM2在AD病理中的独特功能，并重点介绍了TREM2基因的调控。我们还讨论了TREM2对阿尔茨海默氏病中β淀粉样蛋白斑块和tau病理的影响。
关键词: 阿尔茨海默病、TREM2、β淀粉样斑块、tau病理学、小胶质细胞、神经元变性
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