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Basic Science and Pathogenesis.

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Genetic variants in renin-angiotensin systems (RAAS) may influence Alzheimer's disease (AD) risk differently across racial groups. Specific RAAS gene variations interacting with APOE influence AD outcomes, suggesting personalized risk prediction strategies.

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Area of Science:

  • Genetics
  • Neuroscience
  • Public Health

Background:

  • Alzheimer's disease (AD) and related dementias (ADRD) lack a single cause, with risk factors like the APOE ε4 allele and vascular disorders varying in impact across racial/ethnic groups.
  • Vascular health significantly influences cognitive function and neurodegeneration, with genetic variants in the renin-angiotensin aldosterone system (RAAS) playing a role in vascular disease risk.
  • Potential interactions between RAAS genes and APOE suggest RAAS genes are candidates for studying gene-gene interactions in AD/ADRD risk.

Purpose of the Study:

  • To investigate population-specific single nucleotide polymorphisms (SNPs) in RAAS genes associated with vascular disease and AD/ADRD.
  • To explore potential epistatic interactions between RAAS genetic loci and the APOE gene in contributing to AD risk and neurological dysfunction disparities.
  • To identify genetic factors that explain differences in AD risk and outcomes across diverse racial/ethnic populations.

Main Methods:

  • Genomic association analysis was performed on the Healthy Aging Brain Study-Health Disparities (HABS-HD) dataset.
  • RAAS gene variants linked to vascular disorders were identified in Mexican-American, Black, and Non-Hispanic White populations.
  • Epistasis, allele frequency, and genotype distribution analyses were conducted to examine gene-gene interactions and their impact on comorbidity-based AD/ADRD risk.

Main Results:

  • Specific SNPs in ACE1 and AGT loci were identified as candidates for further translational and in vitro studies on epistasis.
  • Unique SNPs associated with distinct phenotypes were found within each racial/ethnic cohort.
  • These findings suggest that gene-gene interactions involving RAAS loci may contribute to differential AD outcomes.

Conclusions:

  • This study highlights the importance of considering disease comorbidity and gene-gene interactions, particularly the interplay between RAAS gene SNPs and APOE, for predicting AD risk.
  • The findings support the need for future mechanistic studies to investigate cellular phenotypes associated with epistatic effects.
  • Understanding these genetic interactions can contribute to developing more precise strategies for AD risk assessment and prevention in diverse populations.