Expressive

rs11030380 - METTL15 - LINC02758

Magnitude 2.2 · 2 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

  • Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use - Unknown journal (n.d.) · Unknown authors · PubMed 30643251

    ABSTRACT: Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders. They are heritable and etiologically related behaviors that have been resistant to gene discovery efforts. In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association. Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco an

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