Expressive

rs10460051 - ASXL3 - NOL4

Magnitude 4.5 · 4 studies on file

Reported associations

  • Depression pathophysiology, risk prediction of recurrence and comorbid psychiatric disorders using genome-wide analyses. - Nature medicine (2023) · Als TD, Kurki MI, Grove J, Voloudakis G, Therrien K, Tasanko E, Nielsen TT, Naamanka J, Veerapen K, Levey DF, Bendl J, Bybjerg-Grauholm J, Zeng B, Demontis D, Rosengren A, Athanasiadis G, Bækved-Hansen M, Qvist P, Bragi Walters G, Thorgeirsson T, Stefánsson H, Musliner KL, Rajagopal VM, Farajzadeh L, Thirstrup J, Vilhjálmsson BJ, McGrath JJ, Mattheisen M, Meier S, Agerbo E, Stefánsson K, Nordentoft M, Werge T, Hougaard DM, Mortensen PB, Stein MB, Gelernter J, Hovatta I, Roussos P, Daly MJ, Mors O, Palotie A, Børglum AD · PubMed 37464041

    Depression is a common psychiatric disorder and a leading cause of disability worldwide. Here we conducted a genome-wide association study meta-analysis of six datasets, including >1.3 million individuals (371,184 with depression) and identified 243 risk loci. Overall, 64 loci were new, including genes encoding glutamate and GABA receptors, which are targets for antidepressant drugs. Intersection with functional genomics data prioritized likely causal genes and revealed new enrichment of prenatal GABAergic neurons, astrocytes and oligodendrocyte lineages. We found depression to be highly polygenic, with ~11,700 variants explaining 90% of the single-nucleotide polymorphism heritability, estimating that >95% of risk variants for other psychiatric disorders (anxiety, schizophrenia, bipolar di

  • Genetic and neural bases of the neuroticism general factor. - Biological psychology (2023) · Kim Y, Saunders GRB, Giannelis A, Willoughby EA, DeYoung CG, Lee JJ · PubMed 37783279

    We applied structural equation modeling to conduct a genome-wide association study (GWAS) of the general factor measured by a neuroticism questionnaire administered to ∼380,000 participants in the UK Biobank. We categorized significant genetic variants as acting either through the neuroticism general factor, through other factors measured by the questionnaire, or through paths independent of any factor. Regardless of this categorization, however, significant variants tended to show concordant associations with all items. Bioinformatic analysis showed that the variants associated with the neuroticism general factor disproportionately lie near or within genes expressed in the brain. Enriched gene sets pointed to an underlying biological basis associated with brain development, synaptic fun

  • Meta-analysis of genome-wide association studies for neuroticism in 449,484 individuals identifies novel genetic loci and pathways. - Nature genetics (2019) · Nagel M, Jansen PR, Stringer S, Watanabe K, de Leeuw CA, Bryois J, Savage JE, Hammerschlag AR, Skene NG, Muñoz-Manchado AB, White T, Tiemeier H, Linnarsson S, Hjerling-Leffler J, Polderman TJC, Sullivan PF, van der Sluis S, Posthuma D · PubMed 29942085

    Neuroticism is an important risk factor for psychiatric traits, including depression , anxiety , and schizophrenia . At the time of analysis, previous genome-wide association studies (GWAS) reported 16 genomic loci associated to neuroticism . Here we conducted a large GWAS meta-analysis (n = 449,484) of neuroticism and identified 136 independent genome-wide significant loci (124 new at the time of analysis), which implicate 599 genes. Functional follow-up analyses showed enrichment in several brain regions and involvement of specific cell types, including dopaminergic neuroblasts (P = 3.49 × 10 ), medium spiny neurons (P = 4.23 × 10 ), and serotonergic neurons (P = 1.37 × 10 ). Gene set analyses implicated three specific pathways: neurogenesis (P = 4.43

  • Item-level analyses reveal genetic heterogeneity in neuroticism - Unknown journal (n.d.) · Unknown authors · PubMed 29500382

    ABSTRACT: Genome-wide association studies (GWAS) of psychological traits are generally conducted on (dichotomized) sums of items or symptoms (e.g., case-control status), and not on the individual items or symptoms themselves. We conduct large-scale GWAS on 12 neuroticism items and observe notable and replicable variation in genetic signal between items. Within samples, genetic correlations among the items range between 0.38 and 0.91 (mean rg = .63), indicating genetic heterogeneity in the full item set. Meta-analyzing the two samples, we identify 255 genome-wide significant independent genomic regions, of which 138 are item-specific. Genetic analyses and genetic correlations with 33 external traits support genetic differences between the items. Hierarchical clustering analysis identifi

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