Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.06.30.662316

Hidden structure in polygenic scores and the challenge of disentangling ancestry interactions in admixed populations

Abstract

The extent to which genetic effects vary across ancestries remains a central question in human genetics, with direct implications for improving polygenic prediction. Recent studies have found that average causal effects are similar across ancestries, but empirical evidence and theoretical considerations suggest that interactions may still contribute to poor portability of polygenic scores. Here, we leverage the ancestry mosaicism of admixed individuals to develop models of genetic interactions with local and global ancestry. We show that these models capture epistasis but are also consistent with highly similar average causal effects, clarifying that the latter observation does not exclude the possibility of gene-ancestry interaction. Next, we investigate how models of local and global interactions differ in polygenic prediction. Focusing on continuous traits, we show that if causal variants are known and causal effects differ across ancestries, then the global and local models can be differentiated using partial polygenic scores -- scores computed on ancestry-specific genomic segments -- while standard polygenic scores remain indistinguishable under both models. However, if causal variants are unknown, differences in linkage disequilibrium (LD) patterns confound this analysis, and the models are not practically distinguishable without knowledge of the LD between causal and tagging variants. Our findings motivate future developments of model-sensitive strategies for individual-level genetic risk prediction.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Aw, A. J., Mandla, R., Shi, Z., Penn Medicine Biobank,, Pasaniuc, B., Mathieson, I.. 2025-07-04. Hidden structure in polygenic scores and the challenge of disentangling ancestry interactions in admixed populations. https://doi.org/10.1101/2025.06.30.662316

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Large language model-based bibliometric evaluation of population descriptors in human genetics

As the use of population descriptors such as race, ethnicity, and ancestry have become increasingly common in modern genetics research, there have been growing calls to critically examine their use. Most notably, in 2023, the National Academies of Science, Engineering, and Medicine (NASEM) published a report titled Using Population Descriptors in Genetics and Genomics Research: A New Framework for an Evolving Field, which included eight specific and actionable recommendations for researchers to implement the ethical and accurate use of population descriptors in genetic research. Here, we use the 2023 NASEM report as a benchmark to analyze the use of population descriptors in genome-wide association studies (GWAS). We develop a general toolkit for large language model-based bibliometrics, operationalize the report's recommendations into an evaluation framework, and apply this framework to evaluate all 4,007 papers from the GWAS Catalog published between 2007 and 2025 with full text available on PubMedCentral. We find significant improvements in adherence to NASEM report recommendations over time. However, most improvements predate the publication of the NASEM report itself, suggesting the report functioned primarily as a synthesis of existing best practices rather than a catalyst for change. We conclude by highlighting opportunities for growth in the field of human genetics.

genetics↗

Mitigating biases of rescaling in forward-in-time population genetic simulations

Forward-in-time population genetic simulations are widely used in evolutionary analyses, but simulating large populations and long genomic regions remains computationally demanding. To reduce this cost, parameter rescaling is widely employed, in which the original evolutionary process is approximated by one with a smaller population size and fewer generations. Recently, several studies using the SLiM simulator have raised concerns about the accuracy of this rescaling approach. In this study, we show that many of the biases reported in these studies can be mitigated by using a different simulation algorithm. These results reveal that the accuracy of parameter rescaling depends on how well the simulation algorithm preserves diffusion-limit properties under rescaling.

genetics↗

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗