4.6 Article

Identification of Biomarkers Related to M2 Macrophage Infiltration in Alzheimer's Disease

期刊

CELLS
卷 11, 期 15, 页码 -

出版社

MDPI
DOI: 10.3390/cells11152365

关键词

Alzheimer's disease; M2 macrophages; toll-like receptor 2; immune infiltration

资金

  1. Zhejiang Provincial Natural Science Foundation of China [LQ21H090005]
  2. National Natural Science Foundation of China [81902604]

向作者/读者索取更多资源

The study confirmed the important role of immune-related mechanisms in Alzheimer's disease and identified hub genes associated with M2 macrophage infiltration. These findings provide new insights into therapeutic strategies for Alzheimer's disease.
Many studies have demonstrated that neuroinflammation contributes to the onset and development of Alzheimer's disease (AD). The infiltration of immune cells in the brain was observed in AD. The purpose of the present study was to verify potential mechanisms and screen out biomarkers related to immune infiltration in AD. We collected the expression profiling datasets of AD patients and healthy donors from the NCBI's Gene Expression Omnibus (GEO) database. We confirmed that immune-related mechanisms were involved in AD using differentially expressed genes analysis and functional enrichment analysis. We then found that M2 macrophage infiltration was most positively correlated with AD according to the CIBERSORT algorithm and a weighted gene co-expression network analysis (WGCNA). TLR2, FCGR2A, ITGB2, NCKAP1L and CYBA were identified as hub genes correlated with M2 macrophage infiltration in AD. Furthermore, the expression levels of these hub genes were positively correlated with A beta 42 and beta-secretase activity. A diagnostic model of these hub genes was constructed, which showed a high area under the curve (AUC) value in both the derivation and validation cohorts. Overall, our work further expanded our understanding of the immunological mechanisms of AD and provided new insights into therapeutic strategies in AD.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据