Expressive

rs10959554 - LINC03131 - JKAMPP1

Magnitude 2.2 · 3 studies on file

Reported associations

  • Genome-wide meta-analysis, functional genomics and integrative analyses implicate new risk genes and therapeutic targets for anxiety disorders. - Nature human behaviour (2024) · Li W, Chen R, Feng L, Dang X, Liu J, Chen T, Yang J, Su X, Lv L, Li T, Zhang Z, Luo XJ · PubMed 37945807

    Anxiety disorders are the most prevalent mental disorders. However, the genetic etiology of anxiety disorders remains largely unknown. Here we conducted a genome-wide meta-analysis on anxiety disorders by including 74,973 (28,392 proxy) cases and 400,243 (146,771 proxy) controls. We identified 14 risk loci, including 10 new associations near CNTNAP5, MAP2, RAB9BP1, BTN1A1, PRR16, PCLO, PTPRD, FARP1, CDH2 and RAB27B. Functional genomics and fine-mapping pinpointed the potential causal variants, and expression quantitative trait loci analysis revealed the potential target genes regulated by the risk variants. Integrative analyses, including transcriptome-wide association study, proteome-wide association study and colocalization analyses, prioritized potential causal genes (including CTNND1 a

  • 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

  • Phenotype integration improves power and preserves specificity in biobank-based genetic studies of major depressive disorder - Unknown journal (n.d.) · Unknown authors · PubMed 37985818

    ABSTRACT: Biobanks often contain several phenotypes relevant to diseases such as major depressive disorder (MDD), with partly distinct genetic architectures. Researchers face complex tradeoffs between shallow (large sample size, low specificity/sensitivity) and deep (small sample size, high specificity/sensitivity) phenotypes, and the optimal choices are often unclear. Here we propose to integrate these phenotypes to combine the benefits of each. We use phenotype imputation to integrate information across hundreds of MDD-relevant phenotypes, which significantly increases genome-wide association study (GWAS) power and polygenic risk score (PRS) prediction accuracy of the deepest available MDD phenotype in UK Biobank, LifetimeMDD. We demonstrate that imputation preserves specificity in its g

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