A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease
Wightman, Douglas P.; Jansen, Iris E.; Savage, Jeanne E.; Shadrin, Alexey; Bahrami, Shahram; Holland, Dominic; Rongve, Arvid; Børte, Sigrid; Winsvold, Bendik K S; Drange, Ole Kristian; Martinsen, Amy E.; Skogholt, Anne Heidi; Willer, Cristen; Bråthen, Geir; Bosnes, Ingunn; Nielsen, Jonas Bille; Fritsche, Lars; Thomas, Laurent; Pedersen, Linda Margareth; Gabrielsen, Maiken Elvestad; Johnsen, Marianne Bakke; Meisingset, Tore Wergeland; Zhou, Wei; Proitsi, Petroula; Hodges, Angela; Dobson, Richard; Velayudhan, Latha; Sealock, Julia; Davis, Lea K.; Pedersen, Nancy L.; Reynolds, Chandra A.; Karlsson, Ida K.; Magnusson, Sigurdur; Stefansson, Hreinn; Thordardottir, Steinunn; Jónsson, Pálmi V.; Snædal, Jon; Zettergren, Anna; Skoog, Ingmar; Kern, Silke; Waern, Margda; Zetterberg, Henrik; Blennow, Kaj; Stordal, Eystein; Hveem, Kristian; Zwart, John Anker Henrik; Athanasiu, Lavinia; Selnes, Per; Saltvedt, Ingvild; Sando, Sigrid Botne; Ulstein, Ingun; Djurovic, Srdjan; Fladby, Tormod; Aarsland, Dag; Selbæk, Geir; Ripke, Stephan; Stefánsson, Kári; Andreassen, Ole; Posthuma, Danielle
Journal article, Peer reviewed
Published version
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https://hdl.handle.net/11250/2825853Utgivelsesdato
2021Metadata
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Originalversjon
10.1038/s41588-021-00921-zSammendrag
Late-onset Alzheimer’s disease is a prevalent age-related polygenic disease that accounts for 50–70% of dementia cases. Currently, only a fraction of the genetic variants underlying Alzheimer’s disease have been identified. Here we show that increased sample sizes allowed identification of seven previously unidentified genetic loci contributing to Alzheimer’s disease. This study highlights microglia, immune cells and protein catabolism as relevant to late-onset Alzheimer’s disease, while identifying and prioritizing previously unidentified genes of potential interest. We anticipate that these results can be included in larger meta-analyses of Alzheimer’s disease to identify further genetic variants that contribute to Alzheimer’s pathology.