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Search: WFRF:(Harder C. B.) > (2020-2023) > Genome-wide analysi...

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FältnamnIndikatorerMetadata
00004646naa a2201105 4500
001oai:prod.swepub.kib.ki.se:148678472
003SwePub
008240701s2022 | |||||||||||000 ||eng|
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1486784722 URI
024a https://doi.org/10.1038/s41588-021-00990-02 DOI
040 a (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Hautakangas, H4 aut
2451 0a Genome-wide analysis of 102,084 migraine cases identifies 123 risk loci and subtype-specific risk alleles
264 c 2022-02-03
264 1b Springer Science and Business Media LLC,c 2022
520 a Migraine affects over a billion individuals worldwide but its genetic underpinning remains largely unknown. Here, we performed a genome-wide association study of 102,084 migraine cases and 771,257 controls and identified 123 loci, of which 86 are previously unknown. These loci provide an opportunity to evaluate shared and distinct genetic components in the two main migraine subtypes: migraine with aura and migraine without aura. Stratification of the risk loci using 29,679 cases with subtype information indicated three risk variants that seem specific for migraine with aura (in HMOX2, CACNA1A and MPPED2), two that seem specific for migraine without aura (near SPINK2 and near FECH) and nine that increase susceptibility for migraine regardless of subtype. The new risk loci include genes encoding recent migraine-specific drug targets, namely calcitonin gene-related peptide (CALCA/CALCB) and serotonin 1F receptor (HTR1F). Overall, genomic annotations among migraine-associated variants were enriched in both vascular and central nervous system tissue/cell types, supporting unequivocally that neurovascular mechanisms underlie migraine pathophysiology.
700a Winsvold, BS4 aut
700a Ruotsalainen, SE4 aut
700a Bjornsdottir, G4 aut
700a Harder, AVE4 aut
700a Kogelman, LJA4 aut
700a Thomas, LF4 aut
700a Noordam, R4 aut
700a Benner, C4 aut
700a Gormley, P4 aut
700a Artto, V4 aut
700a Banasik, K4 aut
700a Bjornsdottir, A4 aut
700a Boomsma, D4 aut
700a Brumpton, B4 aut
700a Burgdorf, KS4 aut
700a Buring, JE4 aut
700a Chalmer, MA4 aut
700a de Boer, I4 aut
700a Dichgans, M4 aut
700a Erikstrup, C4 aut
700a Farkkila, M4 aut
700a Garbrielsen, ME4 aut
700a Ghanbari, M4 aut
700a Hagen, K4 aut
700a Happola, P4 aut
700a Hottenga, JJ4 aut
700a Hrafnsdottir, MG4 aut
700a Hveem, K4 aut
700a Johnsen, MB4 aut
700a Kahonen, M4 aut
700a Kristoffersen, ES4 aut
700a Kurth, T4 aut
700a Lehtimaki, T4 aut
700a Lighart, L4 aut
700a Magnusson, SH4 aut
700a Malik, R4 aut
700a Pedersen, OB4 aut
700a Pelzer, N4 aut
700a Penninx, BWJH4 aut
700a Ran, Cu Karolinska Institutet4 aut
700a Ridker, PM4 aut
700a Rosendaal, FR4 aut
700a Sigurdardottir, GR4 aut
700a Skogholt, AH4 aut
700a Sveinsson, OA4 aut
700a Thorgeirsson, TE4 aut
700a Ullum, H4 aut
700a Vijfhuizen, LS4 aut
700a Widen, E4 aut
700a van Dijk, KW4 aut
700a Aromaa, A4 aut
700a Belin, ACu Karolinska Institutet4 aut
700a Freilinger, T4 aut
700a Ikram, MA4 aut
700a Jarvelin, MR4 aut
700a Raitakari, OT4 aut
700a Terwindt, GM4 aut
700a Kallela, M4 aut
700a Wessman, M4 aut
700a Olesen, J4 aut
700a Chasman, D4 aut
700a Nyholt, DR4 aut
700a Stefansson, H4 aut
700a Stefansson, K4 aut
700a van den Maagdenberg, AMJM4 aut
700a Hansen, TF4 aut
700a Ripatti, S4 aut
700a Zwart, JA4 aut
700a Palotie, A4 aut
700a Pirinen, M4 aut
710a Karolinska Institutet4 org
773t Nature geneticsd : Springer Science and Business Media LLCg 54:2, s. 152-+q 54:2<152-+x 1546-1718x 1061-4036
856u https://www.nature.com/articles/s41588-021-00990-0.pdf
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:148678472
8564 8u https://doi.org/10.1038/s41588-021-00990-0

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