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Basic Science and Pathogenesis.

Ehsan Pishva1, Valentin Laroche2, Rachel Cavill1

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This study identified two distinct epigenetic subtypes of late-onset Alzheimer's disease (LOAD) using DNA methylation data. These subtypes show unique immune and neuronal profiles, offering new therapeutic targets for Alzheimer's disease heterogeneity.

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Area of Science:

  • Neuroscience
  • Genomics
  • Immunology

Background:

  • Late-onset Alzheimer's disease (LOAD) exhibits significant heterogeneity, contributing to treatment failures.
  • Molecular subtyping using omics data is crucial for understanding AD heterogeneity beyond traditional classifications.

Purpose of the Study:

  • To identify distinct molecular subtypes of LOAD using genome-wide DNA methylation data.
  • To characterize the cell-type-specific epigenetic profiles and underlying biological mechanisms of identified LOAD subtypes.

Main Methods:

  • Applied data-driven clustering to genome-wide DNA methylation (DNAm) data from 831 post-mortem AD brain samples across three cohorts.
  • Isolated nuclei populations from prefrontal cortex (PFC) tissue to determine cell-type specificity of DNAm profiles.
  • Performed bulk transcriptomic and single-cell microglial analyses to elucidate subtype-specific biological functions.

Main Results:

  • Identified two reproducible epigenetic subtypes of LOAD (LOAD-S1 and LOAD-S2) based on DNAm profiles.
  • LOAD-S1 subtypes are enriched in immune-related processes, indicating chronic immune hyperactivation.
  • LOAD-S2 subtypes are enriched in neuronal and synaptic functions, exhibiting a dynamic inflammatory profile with reparative mechanisms.

Conclusions:

  • The identified subtype-specific immune signatures offer critical insights into LOAD's molecular heterogeneity.
  • These findings highlight potential therapeutic targets tailored to the distinct immune dysregulation patterns in each LOAD subtype.