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Basic Science and Pathogenesis.

Emma S Luckett1,2,3,4, Yasmina Abakkouy2, Luigi Lorenzini1,4

  • 1Amsterdam UMC location VUmc, Amsterdam, Netherlands.

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Polygenic risk scores (PRS) effectively predict brain amyloid burden in preclinical Alzheimer's disease, particularly in the frontal cortex. These genetic markers show potential for identifying individuals at risk, with notable sex differences observed.

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Area of Science:

  • Neurogenetics
  • Alzheimer's Disease Research

Background:

  • Brain amyloid burden variability suggests underlying biological factors.
  • Investigating genetic determinants of amyloid pathology is crucial for understanding Alzheimer's disease (AD).

Purpose of the Study:

  • To assess the association between polygenic risk scores (PRS) and amyloid burden in a preclinical AD cohort.
  • To identify genetic factors influencing amyloid deposition in the brain.

Main Methods:

  • Computed PRS for AD susceptibility and biomarkers (CSF-Aβ42, ptau181) in 867 non-demented participants.
  • Utilized linear regression to analyze associations with amyloid burden (Centiloid), adjusting for covariates.
  • Performed gene mapping and enrichment analysis on top-performing PRS, with sex-specific analyses.

Main Results:

  • PRSamyloid at pT=1x10⁻⁵ showed the strongest prediction for frontal amyloid burden (R²=0.18).
  • PRSamyloid and PRSKunkle demonstrated comparable predictive performance across brain regions at stringent thresholds.
  • Enrichment analysis revealed distinct biological pathways for PRSamyloid (lipid homeostasis) and PRSKunkle (amyloid-related processes).
  • Predictive performance was highest in the frontal cortex and showed stronger associations in males.

Conclusions:

  • Polygenic risk scores, particularly PRSamyloid and PRSKunkle, effectively predict frontal amyloid burden in preclinical AD.
  • These findings highlight the potential of genetic profiling for identifying at-risk individuals.
  • Observed sex differences in predictive performance warrant further investigation into the genetic basis of AD.