We reasoned that H-MAGMA would provide neurobiologically relevant target genes for GWAS by accurately linking non-coding variants to their cognate genes via brain-derived chromatin interaction profiles. We therefore applied the framework to nine brain GWAS, including five neuropsychiatric disorders and four degenerative disorders (Fig. 1a). The number of brain disorder risk genes (FDR<0.05) was comparable between H-MAGMA and cMAGMA (Extended Data Fig. 1b, Supplementary Data 1–2), whereas the number of SNPs assigned per gene was three-fold higher for cMAGMA (~244 SNPs per gene) than H-MAGMA (~73 SNPs per gene, Extended Data Fig. 1c). In total, cMAGMA and H-MAGMA linked 7.4M and 3.9M SNPs to genes, respectively (Extended Data Fig. 1d).
