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Basic Science and Pathogenesis.

Yuen Yan Wong1,2,3, Che-Yuan Wu1,2,3, Daniel K Mori-Fegan1,2,3

  • 1University of Toronto, Toronto, ON, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Genetic variants influence how white matter hyperintensities (WMH) relate to Alzheimer's disease (AD) amyloid biomarkers. A specific single nucleotide polymorphism (SNP) on chromosome 18 modifies this relationship, suggesting a role for small nuclear RNA (snRNA) in AD pathogenesis.

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Area of Science:

  • Neurogenetics
  • Alzheimer's Disease Research
  • Vascular Neurology

Background:

  • Brain white matter hyperintensities (WMH) are common in Alzheimer's disease (AD) and linked to amyloid levels.
  • The molecular mechanisms connecting WMH and AD amyloid pathology are not fully understood.

Purpose of the Study:

  • To identify single nucleotide polymorphisms (SNPs) that modify the association between WMH and AD amyloid biomarkers.
  • To elucidate the genetic underpinnings of the WMH-amyloid relationship in AD.

Main Methods:

  • Genome-wide interaction study in ADNI participants, assessing SNP-WMH interactions on CSF Aβ42.
  • Replication in UK Biobank and investigation of SNP-WMH interactions on amyloid pathology in ROSMAP.
  • Utilized automated MRI segmentation for WMH and immunoassays/LC-MS for Aβ42 quantification.

Main Results:

  • A novel 28-variant locus on chromosome 18, with top SNP rs72899960, significantly interacted with WMH to predict CSF Aβ42.
  • This SNP-WMH interaction was replicated in UK Biobank and associated with diffuse plaque burden in ROSMAP.
  • The minor allele of rs72899960 showed a protective effect, correlating with higher Aβ42 and lower plaque burden in individuals with greater WMH.

Conclusions:

  • Genomic variants, particularly involving snRNA, modulate the relationship between WMH and amyloid biomarkers in AD.
  • This highlights a potential regulatory role for snRNA pathways in the interplay between vascular disease and AD pathology.
  • Findings suggest novel therapeutic targets for AD by focusing on snRNA and related pathways.