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Basic Science and Pathogenesis.

Larry D Adams1, Jose J Sanchez1, Vanessa C Rodriguez1

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Summary
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Genetic studies in Cuban Americans replicated Alzheimer disease (AD) risk loci, including APOE4, SPI1, and ADAMTS1. These findings advance understanding of AD genetic architecture across diverse populations.

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Area of Science:

  • Genetics
  • Neuroscience
  • Population Health

Background:

  • Alzheimer disease (AD) genetic studies have identified over 80 loci, with APOE being a major risk factor.
  • Understanding genetic variations across ancestries is crucial for effective AD research and interventions.
  • Cuban Americans possess mixed European, African, and Amerindian ancestries, offering a unique population for genetic studies.

Purpose of the Study:

  • To investigate the association of established Alzheimer disease (AD) risk loci within the Cuban American population.
  • To determine if genetic risk factors for AD are consistent across different ancestral backgrounds.
  • To enhance the understanding of the genetic architecture of Alzheimer disease (AD) in diverse populations.

Main Methods:

  • Utilized data from the Cuban American Alzheimer's Disease Initiative (CuADI) cohort, including 239 individuals.
  • Employed a mixed-model regression approach (SAIGE) for association analysis.
  • Controlled for age, gender, population substructure (principal components), and relatedness in the analysis.

Main Results:

  • Replicated SORL1, CR1, ADAM17, and RASGEF1C as risk loci for Alzheimer disease (AD) in Cuban Americans.
  • Identified SPI1 and ADAMTS1 as protective loci for AD in this population.
  • Confirmed APOE4 as a significant risk factor for AD (OR=2.94, p=1.37×10-4), with an effect size comparable to European populations.

Conclusions:

  • Replicated associations of SORL1, CR1, ADAM17, RASGEF1C, SPI1, and ADAMTS1 with AD risk and protection in Cuban Americans.
  • The significant effect of APOE4 in Cuban Americans aligns with its known role in AD pathogenesis across diverse ancestries.
  • Findings contribute to a broader understanding of AD's genetic underpinnings and support targeted research and interventions.