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Magnusson, P. K. E.

Publications and source records attributed to Magnusson, P. K. E..

6 recordsLinked to original sources

An Updated Polygenic Index Repository: Expanded Phenotypes, New Cohorts, and Improved Causal Inference

Polygenic indexes (PGIs) -- DNA-based predictors of individual phenotypes -- have become essential tools across biomedical and social sciences. We introduce Version 2 of the Polygenic Index Repository, which expands phenotype coverage from 47 to 61, increases the number of participating datasets from 11 to 20, and adopts a more consistent and improved methodology for PGI construction. For 16 phenotypes, we leverage summary statistics from an updated GWAS meta-analysis with greater statistical power compared to the original release, thereby improving the PGIs predictive power. To improve power for family-based analyses, we provide imputed parental PGIs in all datasets with first-degree relatives and offer a framework for interpreting results from analyses that control for parental PGIs. We illustrate the utility of parental PGIs using two applications: (1) comparing PGI associations with and without parental PGI controls for all phenotypes in two Repository datasets with family data, and (2) for BMI and diastolic blood pressure, exploring the contribution of causal versus non-causal components of PGI associations to the imperfect portability of PGIs across subgroups within a genetic ancestry. Collectively, the updates enhance predictive performance, broaden the Repositorys scope, and introduce novel resources that reduce confounding bias and improve interpretability.

genomics↗

Resource Profile and User Guide of the Polygenic Index Repository

Polygenic indexes (PGIs) are DNA-based predictors. Their value for research in many scientific disciplines is rapidly growing. As a resource for researchers, we used a consistent methodology to construct PGIs for 47 phenotypes in 11 datasets. To maximize the PGIs prediction accuracies, we constructed them using genome-wide association studies--some of which are novel--from multiple data sources, including 23andMe and UK Biobank. We present a theoretical framework to help interpret analyses involving PGIs. A key insight is that a PGI can be understood as an unbiased but noisy measure of a latent variable we call the "additive SNP factor." Regressions in which the true regressor is the additive SNP factor but the PGI is used as its proxy therefore suffer from errors-in-variables bias. We derive an estimator that corrects for the bias, illustrate the correction, and make a Python tool for implementing it publicly available.

genomics↗

Association Tests Using Copy Number Profile Curves (CONCUR) Enhances Power in Rare Copy Number Variant Analysis

Copy number variants (CNVs) are the gain or loss of DNA segments in the genome that can vary in dosage and length. CNVs comprise a large proportion of variation in human genomes and impact health conditions. To detect rare CNV association, kernel-based methods have been shown to be a powerful tool because their flexibility in modeling the aggregate CNV effects, their ability to capture effects from different CNV features, and their ability to accommodate effect heterogeneity. To perform a kernel association test, a CNV locus needs to be defined so that locus-specific effects can be retained during aggregation. However, CNV loci are arbitrarily defined and different locus definitions can lead to different performance depending on the underlying effect patterns. In this work, we develop a new kernel-based test called CONCUR (i.e., Copy Number profile Curve-based association test) that is free from a definition of locus and evaluates CNV-phenotype association by comparing individuals copy number profiles across the genomic regions. CONCUR is built on the proposed concepts of \"copy number profile curves\" to describe the CNV profile of an individual, and the \"common area under the curve (cAUC) kernel\" to model the multi-feature CNV effects. Compared to existing methods, CONCUR captures the effects of CNV dosage and length, accounts for the continuous nature of copy number values, and accommodates between- and within-locus etiological heterogeneities without the need to define artificial CNV loci as required in current kernel methods. In a variety of simulation settings, CONCUR shows comparable and improved power over existing approaches. Real data analyses suggest that CONCUR is well powered to detect CNV effects in gene pathways associated with phenotypes using data from the Swedish Schizophrenia Study and the Taiwan Biobank.\n\nAuthor summaryCopy number variants comprise a large proportion of variation in human genomes. Large rare CNVs, especially those disrupting genes or changing the dosages of genes, can carry relatively strong risks for neurodevelopmental and neuropsychiatric disorders. Kernel-based association methods have been developed for the analysis of rare CNVs and shown to be a valuable tool. Kernel methods model the collective effect of rare CNVs using flexible kernel functions that capture the characteristics of CNVs and measure CNV similarity of individual pairs. Typically kernels are created by summarizing similarity within an artificially defined \"CNV locus\" and then collapsing across all loci. In this work, we propose a new kernel-based test, CONCUR, that is based on the CNV location information contained in standard processing of the variants and removes the need for any arbitrarily defined CNV loci. CONCUR quantifies similarity between individual pairs as the common area under their copy number profile curves and is designed to detect CNV dosage, length and dosage-length interaction effects. In simulation studies and real data analysis, we demonstrate the ability of CONCUR test to detect CNV effects under diverse CNV architectures with power and robustness over existing methods.

bioinformatics↗

Levels of histidine-rich glycoprotein in human blood predict accelerated aging

1.Despite recognizing aging as risk factor of human diseases, little is still known about the molecular traits of biological age and mortality risk. To identify age-associated proteins circulating human blood, we screened 156 subjects aged 50-92 years using an exploratory and multiplexed affinity proteomics approach. We corroborated the top age-associated protein profile (adjusted P < 0.001) in eight additional study sets (N = 4,044 individuals), and confirmed a consistent age-associated increase (P = 6.61 x 10-6) by meta-analysis. Applying antibody validation determined circulating histidine-rich glycoprotein (HRG) as the target, and we observed that sequence variants influenced the antibodies ability to bind to the protein. Profiles of circulating HRG were associated to several clinical traits and predicted the risk of mortality during a follow-up period of 8.5 years (IQR = 7.7-9.3 years) after blood sampling (HR = 1.25 per SD; 95% CI = 1.12-1.39; P = 7.41 x 10-5). In conclusion, our affinity proteomics analysis found associations between the molecular traits of circulating HRG with age and all-cause mortality. This suggests that the profiles of multi-purpose protein HRG could serve as an accessible indicator of physiological processes related to aging.

epidemiology↗

Equivalence of LD-Score Regression and Individual-Level-Data Methods

LD-score (LDSC) regression disentangles the contribution of polygenic signal, in terms of SNP-based heritability, and population stratification, in terms of a so-called intercept, to GWAS test statistics. Whereas LDSC regression uses summary statistics, methods like Haseman-Elston (HE) regression and genomic-relatedness-matrix (GRM) restricted maximum likelihood infer parameters such as SNP-based heritability from individual-level data directly. Therefore, these two types of methods are typically considered to be profoundly different. Nevertheless, recent work has revealed that LDSC and HE regression yield near-identical SNP-based heritability estimates when confounding stratification is absent. We now extend the equivalence; under the stratification assumed by LDSC regression, we show that the intercept can be estimated from individual-level data by transforming the coefficients of a regression of the phenotype on the leading principal components from the GRM. Using simulations, considering various degrees and forms of population stratification, we find that intercept estimates obtained from individual-level data are nearly equivalent to estimates from LDSC regression (R2 > 99%). An empirical application corroborates these findings. Hence, LDSC regression is not profoundly different from methods using individual-level data; parameters that are identified by LDSC regression are also identified by methods using individual-level data. In addition, our results indicate that, under strong stratification, there is misattribution of stratification to the slope of LDSC regression, inflating estimates of SNP-based heritability from LDSC regression ceteris paribus. Hence, the intercept is not a panacea for population stratification. Consequently, LDSC-regression estimates should be interpreted with caution, especially when the intercept estimate is significantly greater than one.

genetics↗

Polygenic Link Between Blood Lipids And Amyotrophic Lateral Sclerosis

Dyslipidemia is common among patients with amyotrophic lateral sclerosis (ALS). We aimed to test the association and causality between blood lipids and ALS, using polygenic analyses on the summary results of genome-wide association studies. Polygenic risk scores (PRS) based on low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) risk alleles were significantly associated with a higher risk of ALS. Using single nucleotide polymorphisms (SNPs) specifically associated with LDL-C and TC as the instrumental variables, statistically significant causal effects of LDL-C and TC on ALS risk were identified in Mendelian randomization analysis. No significant association was noted between PRS based on triglycerides or high-density lipoprotein cholesterol risk alleles and ALS, and the PRS based on ALS risk alleles were not associated with any studied lipids. This study supports that high levels of LDL-C and TC are risk factors for ALS, and it also suggests a causal relationship of LDL-C and TC to ALS.

genetics↗