Neurobiology of aging · 2018
An APOE-independent cis-eSNP on chromosome 19q13.32 influences tau levels and late-onset Alzheimer's disease risk.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
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Rao Shuquan, Ghani Mahdi, Guo Zhiyun, Deming Yuetiva, Wang Kesheng, Sims Rebecca, Mao Canquan, Yao Yao, Cruchaga Carlos, Stephan Dietrich A, Rogaeva Ekaterina
Аннотация
Although multiple susceptibility loci for late-onset Alzheimer's disease (LOAD) have been identified, a large portion of the genetic risk for this disease remains unexplained. LOAD risk may be associated with single-nucleotide polymorphisms responsible for changes in gene expression (eSNPs). To detect eSNPs associated with LOAD, we integrated data from LOAD genome-wide association studies and expression quantitative trait loci using Sherlock (a Bayesian statistical method). We identified a cis-regulatory eSNP (rs2927438) located on chromosome 19q13.32, for which subsequent analyses confirmed the association with both LOAD risk and the expression level of several nearby genes. Importantly, rs2927438 may represent an APOE-independent LOAD eSNP according to the weak linkage disequilibrium of rs2927438 with the 2 polymorphisms (rs7412 and rs429358) defining the APOE-ε2, -ε3, and -ε4 alleles. Furthermore, rs2927438 does not influence chromatin interaction events at the APOE locus or cis-regulation of APOE expression. Further exploratory analysis revealed that rs2927438 is significantly associated with tau levels in the cerebrospinal fluid. Our findings suggest that rs2927438 may confer APOE-independent risk for LOAD.
Предметные рубрики MeSH
AllelesAlzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EChromosomes, Human, Pair 19FemaleGene ExpressionGenetic Predisposition to DiseaseGenome-Wide Association StudyHippocampusHumansLinkage DisequilibriumMaleOrgan SizePeptide FragmentsPolymorphism, Single NucleotideQuantitative Trait LociRisktau Proteins