Wild-type sTREM2 blocks Aβ aggregation and neurotoxicity, but the Alzheimer's R47H mutant increases Aβ aggregation.

doi:10.1016/j.jbc.2021.100631

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Article

Wild-type sTREM2 blocks Aβ aggregation and neurotoxicity, but the Alzheimer's R47H mutant increases Aβ aggregation.

The Journal of biological chemistry - 1 Jan 2000

Vilalta Anna, Zhou Ye, Sevalle Jean, Griffin Jennifer K, Satoh Kanayo, Allendorf David H, De Suman, Puigdellívol Mar, Bruzas Arturas, Burguillos Miguel A, Dodd Roger B, Chen Fusheng, Zhang Yalun, Flagmeier Patrick, Needham Lisa-Maria, Enomoto Masahiro, Qamar Seema, Henderson James, Walter Jochen, Fraser Paul E, Klenerman David, Lee Steven F, St George-Hyslop Peter, Brown Guy C

Abstract excerpt

TREM2 is a pattern recognition receptor, expressed on microglia and myeloid cells, detecting lipids and Aβ and inducing an innate immune response. Missense mutations (e.g., R47H) of TREM2 increase risk of Alzheimer's disease (AD). The soluble ectodomain of wild-type TREM2 (sTREM2) has been shown to protect against AD in vivo, but the underlying mechanisms are unclear. We show that Aβ oligomers bind to cellular...

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Identifiers

PMID: 33823153
DOI: 10.1016/j.jbc.2021.100631
PMCID: PMC8113883

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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