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dc.contributor.authorWitoelar, Aree
dc.contributor.authorRongve, Arvid
dc.contributor.authorAlmdahl, Ina Selseth
dc.contributor.authorUlstein, Ingun
dc.contributor.authorEngvig, Andreas
dc.contributor.authorWhite, Linda Rosemary
dc.contributor.authorSelbæk, Geir
dc.contributor.authorStordal, Eystein
dc.contributor.authorAndersen, Fredrik
dc.contributor.authorBrækhus, Anne
dc.contributor.authorSaltvedt, Ingvild
dc.contributor.authorEngedal, Knut
dc.contributor.authorHughes, Timothy
dc.contributor.authorBergh, Sverre
dc.contributor.authorBråthen, Geir
dc.contributor.authorBogdanovic, Nenad
dc.contributor.authorBettella, Francesco
dc.contributor.authorWang, Yunpeng
dc.contributor.authorAthanasiu, Lavinia
dc.contributor.authorBahrami, Shahram
dc.contributor.authorLe Hellard, Stephanie
dc.contributor.authorGiddaluru, Sudheer
dc.contributor.authorDale, Anders M
dc.contributor.authorSando, Sigrid Botne
dc.contributor.authorSteinberg, Stacy
dc.contributor.authorStefansson, Hreinn
dc.contributor.authorSnaedal, Jon
dc.contributor.authorDesikan, Rahul S
dc.contributor.authorStefansson, Kari
dc.contributor.authorAarsland, Dag
dc.contributor.authorDjurovic, Srdjan
dc.contributor.authorFladby, Tormod
dc.contributor.authorAndreassen, Ole Andreas
dc.date.accessioned2020-09-02T12:26:01Z
dc.date.available2020-09-02T12:26:01Z
dc.date.created2019-01-04T13:39:44Z
dc.date.issued2018
dc.identifier.citationScientific Reports. 2018, .en_US
dc.identifier.issn2045-2322
dc.identifier.urihttps://hdl.handle.net/11250/2676062
dc.description.abstractA 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.isoengen_US
dc.publisherNature Researchen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.subjectAdolescent 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 Adulten_US
dc.titleMeta-analysis of Alzheimer’s disease on 9,751 samples from Norway and IGAP study identifies four risk locien_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_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.pagenumber8en_US
dc.source.volume8en_US
dc.source.journalScientific Reportsen_US
dc.source.issue1en_US
dc.identifier.doi10.1038/s41598-018-36429-6
dc.identifier.cristin1650460
dc.relation.projectNorges forskningsråd: 251134en_US
cristin.unitcode1991,9,1,0
cristin.unitnameAvd Alderspsykiatri
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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