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Xiao Fen Chen

Researcher at Xiamen University

Publications -  25
Citations -  2032

Xiao Fen Chen is an academic researcher from Xiamen University. The author has contributed to research in topics: TREM2 & Microglia. The author has an hindex of 17, co-authored 25 publications receiving 1392 citations. Previous affiliations of Xiao Fen Chen include University of California, Los Angeles & Laboratory of Molecular Biology.

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Journal ArticleDOI

Apolipoprotein E Is a Ligand for Triggering Receptor Expressed on Myeloid Cells 2 (TREM2)

TL;DR: It is demonstrated that apoE-TREM2 interaction in microglia plays critical roles in modulating phagocytosis of apo E-bound apoptotic neurons and establish a critical link between two proteins whose genes are strongly linked to the risk for AD.
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Soluble TREM2 induces inflammatory responses and enhances microglial survival

TL;DR: It is shown that sTREM2 promotes microglial survival in a PI3K/Akt-dependent manner and stimulates the production of inflammatory cytokines depending on NF-&kgr;B and this study has implications for the pathogenesis of AD and provides insights into targeting sT REM2 pathway for AD therapy.
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Soluble TREM2 ameliorates pathological phenotypes by modulating microglial functions in an Alzheimer's disease model.

TL;DR: The role of sTREM2 is studied in a mouse model of Alzheimer’s disease, and it is found it reduces amyloid accumulation and increases the numbers of plaque-associated microglia which correlates with improved behavioural function in the mice.
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TREM2 Promotes Microglial Survival by Activating Wnt/β-Catenin Pathway

TL;DR: A critical role of TREM2-mediated Wnt/β-catenin pathway in microglial viability is demonstrated and modulating this pathway therapeutically may help to combat the impaired microglia survival and microgliosis associated with AD.
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Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2).

TL;DR: The 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.