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Basic Science and Pathogenesis.

Alison M Goate1,2,3, Edoardo Marcora3, Alexandra Münch2

  • 1Alzheimer Disease Research Center, New York, NY, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Lower MS4A4A and MS4A6A gene expression in myeloid cells is linked to reduced Alzheimer's disease (AD) risk. These genes influence AD-related pathways and may offer therapeutic targets for lowering AD risk.

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Area of Science:

  • Genomics
  • Neuroscience
  • Immunology

Background:

  • Genome-wide association studies (GWAS) have identified Alzheimer's disease (AD) risk loci but rarely specific genes.
  • Functional genomic approaches are crucial for identifying candidate genes and understanding AD risk mechanisms.

Purpose of the Study:

  • To identify candidate causal genes within AD risk loci using myeloid genomics and epigenomics.
  • To investigate the functional consequences of modulating candidate gene expression in microglia and co-culture models.

Main Methods:

  • Employed myeloid genomics and epigenomics to pinpoint candidate genes in AD risk loci.
  • Utilized induced pluripotent stem cell-derived microglia for in vitro and in vivo functional studies.
  • Investigated gene expression changes and cellular phenotypes in MS4A4A/6A knockout models.

Main Results:

  • Reduced MS4A4A and MS4A6A levels in myeloid cells correlate with decreased AD risk.
  • MS4A4A/6A knockout microglia showed altered enrichment in intracellular transport, catabolic, and immune receptor pathways.
  • These cells exhibited reduced lysosomal mass and influenced TREM2 signaling.

Conclusions:

  • MS4A4A and MS4A6A gene expression impacts AD-associated phenotypes.
  • Modulating MS4A4A/MS4A6A presents a potential therapeutic strategy for reducing AD risk.