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000141624 0247_ $$2doi$$a10.1016/S1474-4422(19)30320-5
000141624 0247_ $$2pmid$$apmid:31701892
000141624 0247_ $$2ISSN$$a1474-4422
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000141624 037__ $$aDZNE-2020-07948
000141624 041__ $$aEnglish
000141624 082__ $$a610
000141624 1001_ $$0P:(DE-HGF)0$$aNalls, Mike A$$b0$$eCorresponding author
000141624 245__ $$aIdentification of novel risk loci, causal insights, and heritable risk for Parkinson's disease: a meta-analysis of genome-wide association studies.
000141624 260__ $$aLondon$$bLancet Publ. Group$$c2019
000141624 264_1 $$2Crossref$$3print$$bElsevier BV$$c2019-12-01
000141624 3367_ $$2DRIVER$$aarticle
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000141624 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1718697595_13421
000141624 3367_ $$2BibTeX$$aARTICLE
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000141624 3367_ $$00$$2EndNote$$aJournal Article
000141624 520__ $$aGenome-wide association studies (GWAS) in Parkinson's disease have increased the scope of biological knowledge about the disease over the past decade. We aimed to use the largest aggregate of GWAS data to identify novel risk loci and gain further insight into the causes of Parkinson's disease.We did a meta-analysis of 17 datasets from Parkinson's disease GWAS available from European ancestry samples to nominate novel loci for disease risk. These datasets incorporated all available data. We then used these data to estimate heritable risk and develop predictive models of this heritability. We also used large gene expression and methylation resources to examine possible functional consequences as well as tissue, cell type, and biological pathway enrichments for the identified risk factors. Additionally, we examined shared genetic risk between Parkinson's disease and other phenotypes of interest via genetic correlations followed by Mendelian randomisation.Between Oct 1, 2017, and Aug 9, 2018, we analysed 7·8 million single nucleotide polymorphisms in 37 688 cases, 18 618 UK Biobank proxy-cases (ie, individuals who do not have Parkinson's disease but have a first degree relative that does), and 1·4 million controls. We identified 90 independent genome-wide significant risk signals across 78 genomic regions, including 38 novel independent risk signals in 37 loci. These 90 variants explained 16-36% of the heritable risk of Parkinson's disease depending on prevalence. Integrating methylation and expression data within a Mendelian randomisation framework identified putatively associated genes at 70 risk signals underlying GWAS loci for follow-up functional studies. Tissue-specific expression enrichment analyses suggested Parkinson's disease loci were heavily brain-enriched, with specific neuronal cell types being implicated from single cell data. We found significant genetic correlations with brain volumes (false discovery rate-adjusted p=0·0035 for intracranial volume, p=0·024 for putamen volume), smoking status (p=0·024), and educational attainment (p=0·038). Mendelian randomisation between cognitive performance and Parkinson's disease risk showed a robust association (p=8·00 × 10-7).These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, to the best of our knowledge, by revealing many additional Parkinson's disease risk loci, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified. These associations derived from European ancestry datasets will need to be followed-up with more diverse data.The National Institute on Aging at the National Institutes of Health (USA), The Michael J Fox Foundation, and The Parkinson's Foundation (see appendix for full list of funding sources).
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000141624 542__ $$2Crossref$$i2019-12-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000141624 588__ $$aDataset connected to CrossRef, PubMed,
000141624 650_2 $$2MeSH$$aDatabases, Genetic
000141624 650_2 $$2MeSH$$aGenetic Loci: genetics
000141624 650_2 $$2MeSH$$aGenetic Predisposition to Disease: epidemiology
000141624 650_2 $$2MeSH$$aGenetic Predisposition to Disease: genetics
000141624 650_2 $$2MeSH$$aGenome-Wide Association Study: methods
000141624 650_2 $$2MeSH$$aHumans
000141624 650_2 $$2MeSH$$aParkinson Disease: diagnosis
000141624 650_2 $$2MeSH$$aParkinson Disease: epidemiology
000141624 650_2 $$2MeSH$$aParkinson Disease: genetics
000141624 650_2 $$2MeSH$$aRisk Factors
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000141624 7001_ $$aBotia, Juan A$$b25
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000141624 7001_ $$aCorvol, Jean-Christophe$$b27
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000141624 7001_ $$aSutherland, Margaret$$b31
000141624 7001_ $$aTienari, Pentti$$b32
000141624 7001_ $$aMajamaa, Kari$$b33
000141624 7001_ $$aToft, Mathias$$b34
000141624 7001_ $$0P:(DE-HGF)0$$aAndreassen, Ole A$$b35
000141624 7001_ $$aBangale, Tushar$$b36
000141624 7001_ $$aBrice, Alexis$$b37
000141624 7001_ $$aYang, Jian$$b38
000141624 7001_ $$aGan-Or, Ziv$$b39
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000141624 7001_ $$aTeam, 23andMe Research$$b51
000141624 7001_ $$aConsortium, System Genomics of Parkinson's Disease$$b52
000141624 7001_ $$aConsortium, International Parkinson's Disease Genomics$$b53
000141624 7001_ $$aAdarmes-Gómez, Astrid D$$b54
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