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Basic Science and Pathogenesis.

Brendan R Tobin1, Sara Bitarafan1, Levi B Wood1

  • 1Georgia Institute of Technology, Atlanta, GA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary

Researchers identified three receptor tyrosine kinase (RTK) ligands—Csf1, Tgfb1, and Gas6—that may drive the destructive disease-associated microglia (DAM) phenotype in Alzheimer's Disease (AD). These ligands show therapeutic potential for modulating DAM in AD.

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Microglia in Alzheimer's Disease (AD) shift from a homeostatic to a disease-associated microglia (DAM) phenotype.
  • Hyperactivation of ERK1/2, a protein kinase, has been observed in microglia from AD mouse models.
  • DAM development is a progressive process, with microglia transitioning over time.

Purpose of the Study:

  • To identify receptor tyrosine kinase (RTK) ligands that may drive the transition to the DAM phenotype in Alzheimer's Disease.
  • To investigate the temporal expression patterns of these ligands during DAM development.

Main Methods:

  • Single nucleus RNA sequencing data from a 5xFAD mouse model was analyzed using Seurat.
  • NicheNetR was employed to identify potential driver ligands for differential gene expression in 5xFAD microglia.
  • Monocle3 was used to establish a single-nuclear trajectory to track DAM development over pseudotime.

Main Results:

  • Several RTK ligands, including Csf1, Tgfb1, and Gas6, were identified as likely drivers of the DAM phenotype.
  • Csf1 expression increased early in DAM development and plateaued, consistent with its pro-inflammatory role.
  • Tgfb1 expression decreased early and continued to decline in later stages, aligning with its anti-inflammatory function.

Conclusions:

  • Three RTK ligands (Csf1, Tgfb1, Gas6) were identified as potential temporal drivers of DAM development in Alzheimer's Disease.
  • These ligands exhibit altered expression during the progression of DAM.
  • The identified ligands represent potential therapeutic targets for modulating microglial phenotypes in AD.