9 research outputs found
Comparison of RAPD, RFLP, AFLP and SSR markers for diversity studies in tropical maize inbred lines
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Dynamic Pricing Competition with Unobservable Inventory Levels: A Hidden Markov Model Approach
No full textReference genes for quantitative real-time PCR normalization of Cenostigma pyramidale roots under salt stress and mycorrhizal association
No full textRejection sensitivity and trait anxiety: The indirect effects of regulatory emotional self-efficacy and shyness
No full textMetalinguistic contribution to writing competence: a study of monolingual children in China and bilingual children in Singapore
No full textStructural and Functional Connectivity Changes in the Brain Associated with Shyness but Not with Social Anxiety
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Non-coding variability at the APOE locus contributes to the Alzheimer's risk
Get PDFAlzheimer’s disease (AD) is a leading cause of mortality in the elderly. While the coding
change of APOE-ε4 is a key risk factor for late-onset AD and has been believed to be the only
risk factor in the APOE locus, it does not fully explain the risk effect conferred by the locus.
Here, we report the identification of AD causal variants in PVRL2 and APOC1 regions in
proximity to APOE and define common risk haplotypes independent of APOE-ε4 coding
change. These risk haplotypes are associated with changes of AD-related endophenotypes
including cognitive performance, and altered expression of APOE and its nearby genes in the
human brain and blood. High-throughput genome-wide chromosome conformation capture
analysis further supports the roles of these risk haplotypes in modulating chromatin states
and gene expression in the brain. Our findings provide compelling evidence for additional risk
factors in the APOE locus that contribute to AD pathogenesis
