Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2).
Li ZhongZongqi WangDaxin WangZhe WangYuka A MartensLinbei WuYing XuKai WangJianguo LiRuizhi HuangDan CanHuaxi XuGuojun BuXiao-Fen ChenPublished in: Molecular neurodegeneration (2018)
Our data establish a critical link between oAβ1-42, a major pathological component of AD, and TREM2, a strong genetic risk factor for AD expressed in microglia, and suggest that such interaction contributes to the pathogenic events in AD by modulating microglial responses.
Keyphrases
- inflammatory response
- neuropathic pain
- lipopolysaccharide induced
- induced apoptosis
- lps induced
- cell cycle arrest
- signaling pathway
- bone marrow
- electronic health record
- dendritic cells
- acute myeloid leukemia
- genome wide
- spinal cord injury
- gene expression
- knee osteoarthritis
- copy number
- cell proliferation
- endoplasmic reticulum stress
- pi k akt
- binding protein