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Basic Science and Pathogenesis.

Penelope Benchek1, Christiane Reitz2, Sven-Thorsten Dietrich3

  • 1Department of Population & Quantitative Health Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.

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This summary is machine-generated.

Genetic studies reveal low shared Alzheimer's disease (AD) risk across diverse ancestry groups. Ancestry-specific genetic factors for AD require further identification.

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Area of Science:

  • Genetics
  • Neuroscience
  • Population Health

Background:

  • Alzheimer's disease (AD) prevalence and genetic risk factors exhibit significant variation across diverse populations, including Non-Hispanic White (NHW), African American (AA), Asian American (AsA), and Hispanic/Latino (HL) groups.
  • Paradoxical differences in the effect size of genes like APOE across ancestries suggest substantial heterogeneity in AD's genetic architecture.
  • Understanding genetic correlations between ancestry groups is crucial for leveraging genetic information across populations.

Purpose of the Study:

  • To estimate ancestry-specific heritability of AD.
  • To quantify the shared genetic architecture of AD across different ancestry groups.
  • To identify the extent of genetic overlap in AD risk among diverse populations.

Main Methods:

  • Utilized the Alzheimer's Disease Genetics Consortium (ADGC) multi-ancestry TOPMED-imputed dataset for analyses.
  • Calculated ancestry-specific heritability and quantified shared AD genetic architecture using bivariate GREML analyses.
  • Employed a method accounting for ancestry-specific genetic architecture, analyzing common variants (MAF>0.05) and adjusting for covariates.

Main Results:

  • SNP-based heritability estimates for AD varied across ancestries: AA (h²=0.13), NHW (h²=0.14), AsA (h²=0.29), and HL (h²=0.48).
  • Shared genetic component (r_g) for AD was generally low to modest across ancestry pairs, ranging from 13% (AA/HL) to 42% (NHW/HL).
  • Specifically, r_g estimates were: AA/HL (0.13), AA/AsA (0.17), HL/AsA (0.21), NHW/HL (0.28), NHW/AsA (0.32), and NHW/HL (0.42).

Conclusions:

  • While AD pathology is consistent, the impact of genetic variations differs significantly across ancestry groups.
  • The study found low to moderate shared genetic components for AD risk across ancestries, suggesting these may be underestimates.
  • Significant ancestry-specific genetic contributors to AD risk remain to be discovered.