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Basic Science and Pathogenesis.

Bilcag Akgun1, Mario Cornejo-Olivas2,3, Pedro R Mena1

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Summary
This summary is machine-generated.

Peruvian genome-wide association study (GWAS) identified a novel Alzheimer disease (AD) risk variant, p.H157Y, specific to Amerindian ancestry. This finding underscores the importance of diverse populations in understanding AD genetics.

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Area of Science:

  • Genetics
  • Neuroscience
  • Population Studies

Background:

  • Genetic diversity in Alzheimer disease (AD) studies is crucial for identifying risk and protective alleles.
  • The Peruvian population, with significant Amerindian ancestry, offers a unique resource for AD genetic research.
  • Previous studies have characterized known AD genetic risk loci.

Purpose of the Study:

  • To conduct a genome-wide association study (GWAS) in the Peruvian population.
  • To characterize known Alzheimer disease (AD) genetic risk loci within this diverse cohort.
  • To identify ancestry-specific genetic variants associated with AD.

Main Methods:

  • Genome-wide association study (GWAS) on Whole Genome Sequencing (WGS) data from 567 individuals (215 AD, 352 controls).
  • Utilized generalized linear mixed models adjusting for covariates and genetic relatedness.
  • Performed linkage disequilibrium (LD) analysis and local ancestry (LA) assessment for significant variants.

Main Results:

  • Replicated known AD loci: APOE4 allele and TREML2 marker (rs60755019).
  • Identified a TREM2 missense variant (p.H157Y) in strong LD with TREML2, located on an Amerindian ancestral background.
  • Observed a higher effect size for APOE in Peruvians compared to non-Hispanic White populations; p.H157Y is rare globally but present in Admixed Americans.

Conclusions:

  • A novel Alzheimer disease (AD) susceptibility variant, p.H157Y, associated with Amerindian ancestry was identified in Peru.
  • The TREM2 variant p.H157Y, previously noted in Han Chinese, may have an ancestry-specific effect.
  • Findings emphasize the value of studying diverse populations to fully elucidate the genetic architecture of AD and its pathogenesis.