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Basic Science and Pathogenesis.

Vivek Ruhela1, Basilio Cieza1, Richard Mayeux2

  • 1Columbia University, New York, NY, USA.

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

This study identified specific gene variants linked to Alzheimer's disease risk in Hispanic and Non-Hispanic White brain samples. These findings highlight ancestry-specific genetic regulation and potential targets for precision medicine.

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Area of Science:

  • Genomics
  • Neuroscience
  • Population Genetics

Background:

  • Expression quantitative trait loci (eQTL) studies enhance understanding of gene regulation in complex diseases like Alzheimer's disease (AD).
  • Limited research exists on eQTL across diverse ethnic groups, necessitating population-specific analyses.
  • Prefrontal cortical brain samples were utilized from the New York Brain Bank.

Purpose of the Study:

  • To identify expression quantitative trait loci (eQTL) across different ethnic groups.
  • To investigate genetic regulatory mechanisms underlying Alzheimer's disease (AD) risk.
  • To assess shared and ancestry-specific genetic variants influencing AD.

Main Methods:

  • RNA-Seq data from 32 Hispanic and 263 Non-Hispanic White (NHW) prefrontal cortical brain samples were analyzed.
  • Stratified cis- and trans-eQTL analyses were performed using TensorQTL.
  • Genome-Wide Association Study (GWAS) and eCAVIAR were employed to assess genetic colocalization and identify causal variants.

Main Results:

  • A cis-eQTL and GWAS signal colocalization was observed for the EHD1 gene in Hispanic brains (rs755980338, posterior probability = 0.9947).
  • Strong trans-eQTL and GWAS signal colocalization was identified for TMEM68 and DEFA10P in NHW brains (rs7840855, posterior probability = 0.7).
  • These findings indicate shared causal variants with functional relevance in AD risk.

Conclusions:

  • Population-stratified eQTL and colocalization analyses are crucial for understanding complex disease genetics.
  • EHD1, TMEM68, and DEFA10P may play ancestry-specific roles in Alzheimer's disease pathogenesis.
  • Insights into AD genetic architecture can inform precision medicine strategies across diverse populations.