Finemap-MiXeR: A variational Bayesian approach for genetic finemapping

PLoS Genet. 2024 Aug 15;20(8):e1011372. doi: 10.1371/journal.pgen.1011372. eCollection 2024 Aug.

Abstract

Genome-wide association studies (GWAS) implicate broad genomic loci containing clusters of highly correlated genetic variants. Finemapping techniques can select and prioritize variants within each GWAS locus which are more likely to have a functional influence on the trait. Here, we present a novel method, Finemap-MiXeR, for finemapping causal variants from GWAS summary statistics, controlling for correlation among variants due to linkage disequilibrium. Our method is based on a variational Bayesian approach and direct optimization of the Evidence Lower Bound (ELBO) of the likelihood function derived from the MiXeR model. After obtaining the analytical expression for ELBO's gradient, we apply Adaptive Moment Estimation (ADAM) algorithm for optimization, allowing us to obtain the posterior causal probability of each variant. Using these posterior causal probabilities, we validated Finemap-MiXeR across a wide range of scenarios using both synthetic data, and real data on height from the UK Biobank. Comparison of Finemap-MiXeR with two existing methods, FINEMAP and SuSiE RSS, demonstrated similar or improved accuracy. Furthermore, our method is computationally efficient in several aspects. For example, unlike many other methods in the literature, its computational complexity does not increase with the number of true causal variants in a locus and it does not require any matrix inversion operation. The mathematical framework of Finemap-MiXeR is flexible and may also be applied to other problems including cross-trait and cross-ancestry finemapping.

MeSH terms

  • Algorithms*
  • Bayes Theorem*
  • Genome-Wide Association Study* / methods
  • Humans
  • Linkage Disequilibrium*
  • Models, Genetic
  • Polymorphism, Single Nucleotide / genetics
  • Quantitative Trait Loci

Grants and funding

The authors were funded the South-Eastern Norway Regional Health Authority (#2022073 to B.C.A. and O.F.), Research Council of Norway (#324499 to O.F. and #326813 to A.S.), Norway grant (#EEA-RO-NO-2018-0573 to A.S.) and NordForsk to the NeIC Heilsa “Tryggvedottir” (#101021 to B.C.A. and E.H). This research has been conducted using the UK Biobank Resource under Application Number 27412. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.