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Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies
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Biomarkers.

Mario Tranfa1, Leonard Pieperhoff1, Giuseppe Pontillo1,2,3

  • 1Amsterdam University Medical Center (Amsterdam UMC), Amsterdam, North Holland, Netherlands.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Polygenic risk scores for Alzheimer's disease (AD) influence white matter (WM) integrity. Genetic susceptibility interacts with AD pathology, affecting WM fiber density and cross-section through distinct biological pathways.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biomarkers

Background:

  • Alzheimer's disease (AD) diagnosis is shifting towards biological markers like amyloid-β1-42 (Aβ1-42) and phosphorylated-Tau181 (p-Tau181).
  • Not all individuals with Aβ1-42 deposition progress to AD, suggesting other factors influence disease susceptibility.
  • Polygenic pathways and their interaction with AD pathology may explain variability in brain susceptibility.

Purpose of the Study:

  • To investigate the impact of pathway-specific polygenic risk scores (PRSs) on white matter (WM) integrity.
  • To explore the interaction between AD pathology (Aβ1-42, p-Tau181) and PRSs in modulating WM fiber density (FD) and fiber cross-section (FC).
  • To utilize a fixel-based approach for analyzing WM changes in relation to genetic risk and AD biomarkers.

Main Methods:

  • Analysis of 803 non-demented participants from the European Prevention of Alzheimer's Dementia (EPAD) cohort.
  • Genome sequencing, cerebrospinal fluid (CSF) Aβ1-42 and p-Tau181 measurements, and diffusion MRI were performed.
  • Pathway-specific PRSs were constructed based on AD-associated genetic variants grouped by biological function. Linear models assessed effects on FD and FC, corrected for covariates and multiple comparisons.

Main Results:

  • p-Tau181 exhibited a multiphasic relationship with FD.
  • The migration pathway PRS was associated with increased FD and FC, particularly in the left hemisphere.
  • Aβ1-42 and p-Tau181 moderated the effects of clearance and immune activation pathway PRSs on FD, respectively, demonstrating pathology-dependent genetic influences.

Conclusions:

  • Polygenic risk for AD directly impacts WM integrity.
  • Genetic susceptibility to preclinical AD pathology engages specific biological processes that differentially affect WM integrity.
  • Understanding these interactions is crucial for elucidating AD pathogenesis and variability.