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. 2020 Sep 23;11:4799. doi: 10.1038/s41467-020-18534-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a The disease risk of late-onset Alzheimer’s disease of individuals in different deciles of GRS (both GRS_full and GRS_no19), last percentile of GRS_full and in individuals with APOE ɛ2/ɛ2 or ɛ2/ɛ3, APOE ɛ3 homozygotes (ɛ3/ɛ3), APOE ɛ4 heterozygotes (ɛ4/ɛ3 or ɛ4/ɛ2) and APOE ɛ4 homozygotes (ɛ4/ɛ4). Samples from AIBL, Sydney MAS, UKB cases, UKB mother and UKB father were examined. b Odds ratio between individuals in the other deciles and first decile of GRS. GRS_full was calculated based on 1,056,154 HapMap3 SNPs and two APOE SNPs. GRS_no19 was calculated based on HapMap3 SNPs but excluding SNPs from chromosome 19. Only independent (R² < 0.01) SNPs with P < 1 × 10⁻⁸ were used to calculate the GRS. The error bars in b represent 95% confidence interval.