TET2-mutant myeloid cells mitigate Alzheimer's disease progression via CNS infiltration and enhanced phagocytosis in mice.

doi:10.1016/j.stem.2025.06.006

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

TET2-mutant myeloid cells mitigate Alzheimer's disease progression via CNS infiltration and enhanced phagocytosis in mice.

Cell stem cell - 7 Aug 2025

Matatall Katie A, Wathan Trisha K, Nguyen Minh, Chen Hu, McDonald Alexandra, Qi Guantong, Belk Julia A, Florez Marcus A, Le Duy T, Olarinde Temitope, Vlasschaert Caitlyn, Buttigieg Marco M, Fan Chih-Wei, Carcamo Saul, Cao Ruoqiong, Kennedy Daniel E, Maknojia Arushana A, Thatavarty Apoorva, Fernandez Sanchez Josaura V, Bouzid Hind, Veeraragavan Surabi, Crocker Susan, Goodell Margaret A, Rodriguez Antony, Jaiswal Siddhartha, Rauh Michael J, Papapetrou Eirini P, Marro Samuele G, King Katherine Y

Abstract excerpt

Clonal hematopoiesis (CH) is associated with many age-related diseases, but its interaction with Alzheimer's disease (AD) remains unclear. Here, we show that TET2-mutant CH is associated with a 47% reduced risk of late-onset AD (LOAD) in the UK Biobank, whereas other drivers of CH do not confer protection. In a mouse model of AD, transplantation of Tet2-mutant bone marrow reduced cognitive decline and β-amyloid...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Central Nervous System

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Clonal Hematopoiesis

Share to Dioxygenases

Share to DNA Methyltransferase 3A

Share to Microglia

Share to Myeloid Cells

Share to Phagocytosis

Share to Proto-Oncogene Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 40609533
DOI: 10.1016/j.stem.2025.06.006
PMCID: PMC12233156

Genes

TET2
DNMT3A

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TET2-mutant myeloid cells mitigate Alzheimer's disease progression via CNS infiltration and enhanced phagocytosis in mice.PMID 40609533Read ↗

Deciphering the cell-intrinsic effect of DNMT3A clonal hematopoiesis in circulating monocytes: potential mechanistic insights into a protective role in Alzheimer’s diseaseSemantic proximity Read ↗

Mutation-resolved single-cell transcriptomics reveals enhanced β-amyloid clearance in TET2-mutant human monocytes.Semantic proximity Read ↗

Gene expression and functional deficits underlie TREM2-knockout microglia responses in human models of Alzheimer's disease.Semantic proximity Read ↗

Clonal Hematopoiesis in Nonmalignant Disease: Functional Consequences of Mutated Immune Cells by Clonal Hematopoiesis in the Diseased Tissue.Semantic proximity Read ↗

Plasticity of Human Microglia and Brain Perivascular Macrophages in Aging and Alzheimer’s DiseaseSemantic proximity Read ↗

Prior activation state shapes the microglia response to antihuman TREM2 in a mouse model of Alzheimer's disease.Semantic proximity Read ↗

Landscape of brain myeloid cell transcriptome along the spatiotemporal progression of Alzheimer’s disease reveals distinct sequential responses to Aβ and tauSemantic proximity Read ↗

Monocyte-derived microglia with <i>Dnmt3a</i> mutation cause motor pathology in aging miceSemantic proximity Read ↗

Clonal hematopoiesis is associated with protection from Alzheimer’s diseaseSemantic proximity Read ↗

Mouse and human microglial phenotypes in Alzheimer’s disease are controlled by amyloid plaque phagocytosis through Hif1αSemantic proximity Read ↗

Elevated TREM2 Gene Dosage Reprograms Microglia Responsivity and Ameliorates Pathological Phenotypes in Alzheimer's Disease Models.Semantic proximity Read ↗

Transplantation of wild-type hematopoietic stem and progenitor cells rescue Alzheimer’s disease in a mouse model and highlights the central role of microglia in disease pathogenesisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.