Article

<i>Ms4a4a</i> deficiency ameliorates plaque pa thology in a mouse model of amyloid accumulation

2025-03-10

Abstract excerpt

<h4>Background</h4> Genome-wide association studies for Alzheimer disease (AD) risk have identified a number of genes enriched in microglia, including MS4A4A . Common variants in MS4A4A influence AD risk, MS4A4A expression, TREM2 signaling, and a specific microglial transcriptional state, though the exact role of MS4A4A in AD remains unclear. <h4>Methods</h4> Using a mouse model of amyloid beta (Aβ) accumula...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 167a1523-d8ae-545a-bf99-1403159400a5
DOI: 10.1101/2025.03.06.641917

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

<i>Ms4a4a</i> deficiency ameliorates plaque pa thology in a mouse model of amyloid accumulationDOI 10.1101/2025.03.06.641917Read

<i>Ms4a4a</i> loss reprograms amyloid-associated microglia and limits dense-core plaque-associated tau spreadingSemantic proximity Read

The Alzheimer’s Disease Risk Genes MS4A4A And MS4A6A Cooperate to Negatively Regulate Trem2 and Microglia statesSemantic proximity Read

MS4A4A modifies the risk of Alzheimer disease by regulating lipid metabolism and immune response in a unique microglia stateSemantic proximity Read

The <i>MS4A</i> gene cluster is a key regulator of soluble TREM2 and Alzheimer disease riskSemantic proximity Read

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

APOE4 confers transcriptomic and functional alterations to primary mouse microglia.Semantic proximity Read

APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathologySemantic proximity Read

Variants in the MS4A cluster interact with soluble TREM2 expression on biomarkers of neuropathology.Semantic proximity Read

APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathologySemantic proximity Read

A Trem2*R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaquesSemantic proximity Read

TLR4 mutation reduces microglial activation, increases Aβ deposits and exacerbates cognitive deficits in a mouse model of Alzheimer's disease.Semantic proximity Read

DNA hypomethylation promotes the expression of CASPASE-4 which exacerbates neuroinflammation and amyloid-β deposition in Alzheimer’s disease The Ohio State University College of MedicineSemantic proximity Read