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Basic Science and Pathogenesis.

Yuchen Yang1, Haimeng Bai2, Penelope Benchek3

  • 1Case Western Reserve University, Cleveland, OH, USA.

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Summary
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A structural variant in haptoglobin (HP) modifies Alzheimer's disease (AD) risk associated with apolipoprotein E (APOE) alleles. This interaction effect was confirmed in independent datasets, highlighting HP's role in AD pathogenesis.

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Area of Science:

  • Neurogenetics
  • Molecular Biology
  • Disease Pathogenesis

Background:

  • Alzheimer's disease (AD) risk is influenced by genetic factors, including apolipoprotein E (APOE) genotypes.
  • A structural variant (SV) in haptoglobin (HP) has been implicated in modifying AD risk.
  • HP interacts with APOE in human AD brain tissue and binds amyloid-beta in vitro.

Purpose of the Study:

  • To replicate and validate the interaction between HP structural variants and APOE genotypes on AD risk in independent cohorts.
  • To investigate the influence of HP2 allele dosage on APOE-associated AD risk.
  • To confirm previous findings in array-genotyped European-descent cohorts using whole-genome sequenced non-Hispanic White (NHW) and African-American (AFR) datasets.

Main Methods:

  • Imputation of HP1/HP2 alleles from whole-genome sequencing data in NHW and AFR cohorts.
  • Logistic regression modeling to assess AD associations and HP-by-APOE interactions.
  • Stratified analysis by APOE allele carrier status to evaluate interaction effects.

Main Results:

  • The HP2 allele frequency was 0.38 in NHW and 0.59 in AFR.
  • Significant interaction between HP2 and APOE genotypes on AD risk was detected, with increased HP2 allele count modifying APOE ε4 risk and APOE ε2 protection.
  • The strongest interaction effect was observed in APOE ε2 carriers, and AD risk was lowest in individuals homozygous for both APOE ε2 and HP2.

Conclusions:

  • A structural variant of HP significantly modifies the risk effects of APOE alleles on Alzheimer's disease.
  • These findings in independent datasets corroborate the previously discovered interaction between HP and APOE in AD pathogenesis.
  • The study underscores the importance of considering combined genetic effects for a comprehensive understanding of AD risk.