dc.contributor.author | Witoelar, Aree | |
dc.contributor.author | Rongve, Arvid | |
dc.contributor.author | Almdahl, Ina Selseth | |
dc.contributor.author | Ulstein, Ingun | |
dc.contributor.author | Engvig, Andreas | |
dc.contributor.author | White, Linda Rosemary | |
dc.contributor.author | Selbæk, Geir | |
dc.contributor.author | Stordal, Eystein | |
dc.contributor.author | Andersen, Fredrik | |
dc.contributor.author | Brækhus, Anne | |
dc.contributor.author | Saltvedt, Ingvild | |
dc.contributor.author | Engedal, Knut | |
dc.contributor.author | Hughes, Timothy | |
dc.contributor.author | Bergh, Sverre | |
dc.contributor.author | Bråthen, Geir | |
dc.contributor.author | Bogdanovic, Nenad | |
dc.contributor.author | Bettella, Francesco | |
dc.contributor.author | Wang, Yunpeng | |
dc.contributor.author | Athanasiu, Lavinia | |
dc.contributor.author | Bahrami, Shahram | |
dc.contributor.author | Le Hellard, Stephanie | |
dc.contributor.author | Giddaluru, Sudheer | |
dc.contributor.author | Dale, Anders M | |
dc.contributor.author | Sando, Sigrid Botne | |
dc.contributor.author | Steinberg, Stacy | |
dc.contributor.author | Stefansson, Hreinn | |
dc.contributor.author | Snaedal, Jon | |
dc.contributor.author | Desikan, Rahul S | |
dc.contributor.author | Stefansson, Kari | |
dc.contributor.author | Aarsland, Dag | |
dc.contributor.author | Djurovic, Srdjan | |
dc.contributor.author | Fladby, Tormod | |
dc.contributor.author | Andreassen, Ole Andreas | |
dc.date.accessioned | 2020-09-02T12:26:01Z | |
dc.date.available | 2020-09-02T12:26:01Z | |
dc.date.created | 2019-01-04T13:39:44Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Scientific Reports. 2018, . | en_US |
dc.identifier.issn | 2045-2322 | |
dc.identifier.uri | https://hdl.handle.net/11250/2676062 | |
dc.description.abstract | A large fraction of genetic risk factors for Alzheimer's Disease (AD) is still not identified, limiting the understanding of AD pathology and study of therapeutic targets. We conducted a genome-wide association study (GWAS) of AD cases and controls of European descent from the multi-center DemGene network across Norway and two independent European cohorts. In a two-stage process, we first performed a meta-analysis using GWAS results from 2,893 AD cases and 6,858 cognitively normal controls from Norway and 25,580 cases and 48,466 controls from the International Genomics of Alzheimer's Project (IGAP), denoted the discovery sample. Second, we selected the top hits (p < 1 × 10-6) from the discovery analysis for replication in an Icelandic cohort consisting of 5,341 cases and 110,008 controls. We identified a novel genomic region with genome-wide significant association with AD on chromosome 4 (combined analysis OR = 1.07, p = 2.48 x 10-8). This finding implicated HS3ST1, a gene expressed throughout the brain particularly in the cerebellar cortex. In addition, we identified IGHV1-68 in the discovery sample, previously not associated with AD. We also associated USP6NL/ECHDC3 and BZRAP1-AS1 to AD, confirming findings from a follow-up transethnic study. These new gene loci provide further evidence for AD as a polygenic disorder, and suggest new mechanistic pathways that warrant further investigation. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Nature Research | en_US |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/deed.no | * |
dc.subject | Adolescent Adult Aged Alzheimer Disease / genetics* Biomarkers Case-Control Studies Female Genetic Association Studies* / methods Genetic Predisposition to Disease* Humans Male Middle Aged Norway Polymorphism, Single Nucleotide Quantitative Trait Loci* Young Adult | en_US |
dc.title | Meta-analysis of Alzheimer’s disease on 9,751 samples from Norway and IGAP study identifies four risk loci | en_US |
dc.type | Peer reviewed | en_US |
dc.type | Journal article | en_US |
dc.description.version | publishedVersion | en_US |
dc.rights.holder | © The Author(s) 2018.
Open Access This article is licensed under a Creative Commons Attribution 4.0 International
License, which permits use, sharing, adaptation, distribution and reproduction in any medium or
format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Te images or other third party material in this
article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the
material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the
copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. | en_US |
dc.source.pagenumber | 8 | en_US |
dc.source.volume | 8 | en_US |
dc.source.journal | Scientific Reports | en_US |
dc.source.issue | 1 | en_US |
dc.identifier.doi | 10.1038/s41598-018-36429-6 | |
dc.identifier.cristin | 1650460 | |
dc.relation.project | Norges forskningsråd: 251134 | en_US |
cristin.unitcode | 1991,9,1,0 | |
cristin.unitname | Avd Alderspsykiatri | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |