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We first perform a large genetic association study by merging all available case-control datasets and by-proxy study results (discovery <jats:italic>n<\/jats:italic>\u2009=\u2009409,435 and validation size <jats:italic>n<\/jats:italic>\u2009=\u200958,190). Here, we add six variants associated with Alzheimer\u2019s disease risk (near <jats:italic>APP, CHRNE, PRKD3\/NDUFAF7, PLCG2<\/jats:italic> and two exonic variants in the <jats:italic>SHARPIN<\/jats:italic> gene). Assessment of the polygenic risk score and stratifying by <jats:italic>APOE<\/jats:italic> reveal a 4 to 5.5 years difference in median age at onset of Alzheimer\u2019s disease patients in <jats:italic>APOE<\/jats:italic> \u025b4 carriers. Because of this study, the underlying mechanisms of <jats:italic>APP<\/jats:italic> can be studied to refine the amyloid cascade and the polygenic risk score provides a tool to select individuals at high risk of Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.1038\/s41467-021-22491-8","type":"journal-article","created":{"date-parts":[[2021,6,7]],"date-time":"2021-06-07T10:06:06Z","timestamp":1623060366000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":313,"title":["Common variants in Alzheimer\u2019s disease and risk stratification by polygenic risk scores"],"prefix":"10.1038","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2148-381X","authenticated-orcid":false,"given":"Itziar","family":"de 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