Whole-genome sequencing analyses suggest novel genetic factors associated with Alzheimer’s disease and a cumulative effects model for risk liability

Abstract Genome-wide association studies (GWAS) on Alzheimer’s disease (AD) have predominantly focused on identifying common variants in Europeans. Here, we performed whole-genome sequencing (WGS) of 1,559 individuals from a Korean AD cohort to identify various genetic variants and biomarkers associ...

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Main Authors: Jun Pyo Kim, Minyoung Cho, Chanhee Kim, Hyunwoo Lee, Beomjin Jang, Sang-Hyuk Jung, Yujin Kim, In Gyeong Koh, Seoyeon Kim, Daeun Shin, Eun Hye Lee, Jong-Young Lee, YoungChan Park, Hyemin Jang, Bo-Hyun Kim, Hongki Ham, Beomsu Kim, A-Hyun Cho, Towfique Raj, Hee Jin Kim, Duk L. Na, Sang Won Seo, Joon-Yong An, Hong-Hee Won
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-59949-y
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Summary:Abstract Genome-wide association studies (GWAS) on Alzheimer’s disease (AD) have predominantly focused on identifying common variants in Europeans. Here, we performed whole-genome sequencing (WGS) of 1,559 individuals from a Korean AD cohort to identify various genetic variants and biomarkers associated with AD. Our GWAS analysis identified a previously unreported locus for common variants (APCDD1) associated with AD. Our WGS analysis was extended to explore the less-characterized genetic factors contributing to AD risk. We identified rare noncoding variants located in cis-regulatory elements specific to excitatory neurons associated with cognitive impairment. Moreover, structural variation analysis showed that short tandem repeat expansion was associated with an increased risk of AD, and copy number variant at the HPSE2 locus showed borderline statistical significance. APOE ε4 carriers with high polygenic burden or structural variants exhibited severe cognitive impairment and increased amyloid beta levels, suggesting a cumulative effects model of AD risk.
ISSN:2041-1723