This age-dependent change in the direction of the associations observed for cardiometabolic risk factors has been suggested to potentially reflect selection bias, as fatal cardiometabolic disease events would reduce the risk of being diagnosed with Alzheimer’s disease, which usually occurs late in life7. Associations between cardiometabolic risk factors and PRS for Alzheimer’s disease at p≤5×10-1. To test the generalisability of our results, we investigated the characteristics of individuals in the analysis of insulin (model with the fewest individuals and repeated measures) to those excluded from this analysis (individuals with no genetic or cardiometabolic data). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Genome-Wide Polygenic Score, Clinical Risk Factors, and Long-Term Trajectories of Coronary Artery Disease. In agreement with our results, a study found a negative genetic correlation between height and dementia, suggesting our findings for height at liberal thresholds may be due to shared genetic pathways39. We will capitalize on the vast amount of data available in the UK Biobank to provide researchers with a baseline comparison of a healthy European population. Research to understand the spread of the coronavirus, Coronavirus research: how to take a sample, INFORMATION SHEET: UK Biobank coronavirus research, INFORMATION SHEET FOR RELATIVES: UK Biobank coronavirus research, Newsletter 2019 “UK Biobank – the biggest gift ever to science”, Newsletter 2019 Imaging study on course to scan 100,000, Newsletter 2019: A global resource transforming health, Newsletter 2019: Pollution linked with serious changes in the heart. Alongside their report, reviewers assign a status to the article: Biostatistics, Alzheimer's disease genetics. Details about IGAP are in the Extended data17. PLoS medicine 2020 Jul 17(7) e1003152 Details of model selection for each cardiometabolic risk factor. Please disclose any competing interests that might be construed to influence your judgment of the article's or peer review report's validity or importance. Large genetic consortia have identified common genetic variants associated with late-onset Alzheimer’s disease8, with the ε4 allele of the apolipoprotein E (ApoE) gene conferring the greatest risk, increasing the risk up to twelvefold9. To compare fasting/non-fasting biomarkers, we used the PRS excluding ApoE at the genome-wide significant threshold. Measures from the clinic with the highest number of participants were used for the analysis, where applicable. A positive association has also been found for BMI trajectories in midlife and Alzheimer’s disease34. We also found evidence of an association between the PRS for Alzheimer’s disease (including the ApoE region) and HDL, non-HDL, CRP, and triglyceride levels, but the direction of effect was not consistent across all time-points. If applicable, is the statistical analysis and its interpretation appropriate? 3. Variables with a skewed distribution (triglycerides, fat mass, CRP) were (natural) log transformed. The investigators within IGAP contributed to the design and implementation of IGAP and/or provided data but did not participate in analysis or writing of this report. Apart from ApoE, the relationship of these genetic variants to cardiovascular disease is uncertain. You can also read all the peer review reports by downloading the PDF. The predominantly null results at the genome-wide significant p-value threshold may indicate that either the PRS for Alzheimer’s disease does not operate through cardiometabolic pathways or that it operates partly through cardiometabolic pathways, but the associations emerge much later in life. 3 Intro paragraph 2 ‘can be summarised to construct a polygenic risk score’. LMOK was supported by a UK Medical Research Council Population Health Scientist fellowship (MR/M014509/1). Sensitivity analyses comparing the results for the PRS at different p-value thresholds used PRS excluding ApoE. In line with these results, there was little evidence of an association between the PRS, SBP, glucose, triglycerides, non-HDL, HDL-c and CRP (Figure 3). More about the PGS Catalog project, descriptions of the data, and publication eligibility criteria can be found in our documentation and recent preprint.
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