Authors
Maggie Haitian Wang, Yexian Zhang, Rui Sun, Fudong Li, Tao Zhang, Xue Gu, Jingzhi Lou, Lirong Cao, Shimin Su, Hong Zheng, Caiqi Liu, Marc Ka Chun Chong, William Ka Kei Wu, Jun Yu, Benny Chung-Ying Zee, Junfen Lin
Published in
Human genetics. Volume 145. Issue 1. Oct 17, 2026. Epub Oct 17, 2026.
Abstract
While genetic heritability plays a major role in the development of cognitive impairment, most genetic risk factors are identified from studies of European populations. We conducted a genome-wide association study (GWAS) on cognitive impairment in the Chinese population by sequencing 1,040 matched case-control individuals from a longitudinal cohort of Zhejiang Province, China. We detected 19 SNPs clustered in 15 genomic loci reaching suggestive significance (P < 1 × 10- 5). Eleven of these genomic loci are newly associated with Alzheimer's disease (AD) or cognitive impairment, among which five (GRP39, FAT1, EDIL3, ZNF596, and PDGFD) show nominal evidence of replication in both external GWAS of AD in East-Asian populations and summary statistics of AD in diverse populations. The detected loci are implicated in micronutrient homeostasis including zinc (GPR39), iron (STEAP1), potassium (KCNJ6), and vitamin K (VKORC1L1), cell connections (EVPLL) through cadherin regulations (PCDH18, FAT1), regulating amyloid-beta precursor protein (APP) (EDIL3), formation of amyloid-β (EDEM1) and neurofibrillary tangles (PDGFD, ZNF596), neuronal growth (NEGR1), and phosphatase regulations (SETBP1, TPTE). This study presents a robust GWAS for cognitive impairment in the Chinese population and highlights a promising set of therapeutic targets for neurodegenerative disorder.
PMID:
42888346
Bibliographic data and abstract were imported from PubMed on 17 Oct 2026.
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