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Alzheimer's Imaging Consortium.

Ozkan Is1, Jianna Tan1, Jeremiah Bergman1

  • 1Mayo Clinic, Jacksonville, FL, USA.

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Summary
This summary is machine-generated.

This study identifies protective and risk molecular signatures in microglia associated with Alzheimer's disease (AD) genetic variants. These signatures offer potential new therapeutic targets for AD by modulating microglial function.

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alzheimer's disease (AD) involves complex genomic and immunological changes affecting brain cells.
  • Missense variants in microglial genes ABI3 (risk) and PLCG2 (protective) are linked to AD.
  • These gene expression alterations impact microglial function in AD pathogenesis.

Purpose of the Study:

  • To identify protective and risk microglial molecular signatures associated with ABI3 and PLCG2 variants.
  • To determine the role of these signatures in different microglial subtypes and states in AD.
  • To utilize single-cell expression and functional studies for comprehensive analysis.

Main Methods:

  • Generated microglia-enriched single-nucleus RNA sequencing (snRNAseq) data from donors with specific AD-related mutations.
  • Performed differential gene expression (DEG) analysis to define protective (down in ABI3, up in PLCG2) and risk (up in ABI3, down in PLCG2) signatures.
  • Validated signatures across multiple datasets, including iPSC-derived microglia, AD-resilient donors, and external AD cohorts.

Main Results:

  • Identified 227 protective and 293 risk signature genes.
  • Protective genes are downregulated in early AD and upregulated in late AD, correlating with protective variant load.
  • Risk genes are upregulated in early AD, downregulated in late AD and resilient donors, and affected by PLCG2 variant load and Aβ treatment.

Conclusions:

  • Uncovered microglia-specific protective and risk signatures linked to AD genetic variants.
  • These signatures highlight novel immune targets and pathways for therapeutic intervention in AD.
  • Findings have implications for understanding microglial function in neurodegenerative diseases.