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Depositordc.contributorTimmers, Paul
Funderdc.contributor.otherMRC - Medical Research Councilen_UK
Funderdc.contributor.otherUniversity of Edinburghen_UK
Funderdc.contributor.otherWellcome Trusten_UK
Funderdc.contributor.otherAXA Research Fund
Data Creatordc.creatorTimmers, Paul R H J
Data Creatordc.creatorLäll, Kristi
Data Creatordc.creatorFischer, Krista
Data Creatordc.creatorNing, Zheng
Data Creatordc.creatorFeng, Xiao
Data Creatordc.creatorBretherick, Andrew
Data Creatordc.creatorClark, David W
Data Creatordc.creatorShen, Xia
Data Creatordc.creatorEsko, Tōnu
Data Creatordc.creatorKutalik, Zoltán
Data Creatordc.creatorWilson, James F
Data Creatordc.creatorJoshi, Peter K
Date Accessioneddc.date.accessioned2018-11-01T15:10:01Z
Date Availabledc.date.available2019-01-15T05:15:07Z
Citationdc.identifier.citationTimmers, Paul R H J; Läll, Kristi; Fischer, Krista; Ning, Zheng; Feng, Xiao; Bretherick, Andrew; Clark, David W; Shen, Xia; Esko, Tōnu; Kutalik, Zoltán; Wilson, James F; Joshi, Peter K. (2019). Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances, [dataset]. Usher Institute of Population Health Sciences and Informatics. https://doi.org/10.7488/ds/2463.en
Persistent Identifierdc.identifier.urihttp://hdl.handle.net/10283/3209
Persistent Identifierdc.identifier.urihttps://doi.org/10.7488/ds/2463
Dataset Description (abstract)dc.description.abstractWe use a genome-wide association of 1 million parental lifespans of genotyped subjects and data on mortality risk factors to validate previously unreplicated findings near CDKN2B-AS1, ATXN2/BRAP, FURIN/FES, ZW10, PSORS1C3, and 13q21.31, and identify and replicate novel findings near ABO, ZC3HC1, and IGF2R. We also validate previous findings near 5q33.3/EBF1 and FOXO3, whilst finding contradictory evidence at other loci. Gene set and cell-specific analyses show that expression in foetal brain cells and adult dorsolateral prefrontal cortex is enriched for lifespan variation, as are gene pathways involving lipid proteins and homeostasis, vesicle-mediated transport, and synaptic function. Individual genetic variants that increase dementia, cardiovascular disease, and lung cancer – but not other cancers – explain the most variance, possibly reflecting modern susceptibilities, whilst cancer may act through many rare variants, or the environment. Resultant polygenic scores show a mean lifespan difference of around five years of life across the deciles.en_UK
Dataset Description (TOC)dc.description.tableofcontentsSee attached README file for details on the associated data.en_UK
Languagedc.language.isoengen_UK
Publisherdc.publisherUniversity of Edinburgh. Usher Institute of Population Health Sciences and Informaticsen_UK
Relation (Is Referenced By)dc.relation.isreferencedbyhttps://doi.org/10.7554/eLife.39856.001en_UK
Subjectdc.subjectLifespanen_UK
Subjectdc.subjectLongevityen_UK
Subjectdc.subjectMortalityen_UK
Subjectdc.subjectAgeingen_UK
Subjectdc.subjectGWASen_UK
Subjectdc.subjectGWAMAen_UK
Subjectdc.subjectSummary Statisticsen_UK
Subjectdc.subjectSumstatsen_UK
Subject Classificationdc.subject.classificationBiological Sciences::Human Geneticsen_UK
Titledc.titleGenomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chancesen_UK
Alternative Titledc.title.alternativeGenomic underpinnings of lifespan allow prediction and reveal basis in modern risksen_UK
Typedc.typedataseten_UK

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