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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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Alzheimer's Imaging Consortium.

Rafael V Lippert1,2, A Zarina Kraal1,3, Natalie C Edwards1,2

  • 1Columbia University Irving Medical Center, New York, NY, USA.

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

Genetic risk for Alzheimer's disease (AD) is linked to cerebrovascular disease and neurodegeneration markers. White matter hyperintensities mediate this association, impacting cognition even without amyloid presence.

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Area of Science:

  • Neuroscience
  • Genetics
  • Gerontology

Background:

  • Cerebrovascular disease (CVD), inflammation, and neurodegeneration are known risk factors for Alzheimer's disease (AD).
  • Understanding the interplay between genetic predisposition and these pathological factors is crucial for elucidating AD pathogenesis.
  • This study investigates the association between genetic risk for AD and markers of CVD, inflammation, and neurodegeneration in cognitively unimpaired individuals.

Purpose of the Study:

  • To examine the association of an age-anchored polygenic risk score (CIR) with markers of cerebrovascular burden, inflammation, and neurodegeneration.
  • To determine if these factors mediate the relationship between genetic risk and cognitive function.
  • To explore these associations stratified by amyloid-beta (Aβ) positivity.

Main Methods:

  • Utilized data from 601 unimpaired participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI).
  • Assessed white matter hyperintensity (WMH) volumes, CIR scores, plasma GFAP and NfL concentrations, and cognitive performance.
  • Employed linear models for association analyses and mediation analyses to test the role of WMH and biomarkers.

Main Results:

  • Higher CIR scores correlated with increased WMH volume, NfL, and GFAP concentrations.
  • CIR was associated with lower executive function, memory, and language scores.
  • WMH volumes significantly mediated the relationship between CIR and cognitive domains; NfL also mediated executive function.

Conclusions:

  • Elevated genetic risk for AD in cognitively unimpaired older adults is associated with greater cerebrovascular burden and neurodegeneration markers.
  • White matter hyperintensities play a mediating role in linking genetic AD risk to cognitive decline, irrespective of amyloid status.
  • These findings highlight the significant contribution of cerebrovascular disease to the genetic risk of developing clinical Alzheimer's disease.