Expressive

rs11210177 - KRT8P21 - RN7SKP19

Magnitude 2.2 · 3 studies on file

Reported associations

  • Investigating the shared genetic architecture between attention-deficit/hyperactivity disorder and risk taking behavior: A large-scale genomewide cross-trait analysis. - Journal of affective disorders (2024) · Chen Y, Liu P, Yi S, Fan C, Zhao W, Liu J · PubMed 38565336

    This study aims to explore the genetic architecture shared between Attention-Deficit/Hyperactivity Disorder (ADHD) and risk behavior. Based on the latest large-scale Genome-wide association studies (GWAS), we firstly employed Linkage disequilibrium score regression (LDSC) and Local Analysis of Variant Association (LAVA) to investigate the genetic correlation between risk behavior and ADHD. Then, we conducted cross-trait analysis to identified the Pleiotropic loci. Finally, bidirectional Mendelian randomization analysis (MR) was applied to examine the causal relationship. We found a significant positive genetic correlation between ADHD and risk-taking behavior (rg = 0.351, p = 6.50E-37). The cross-trait meta-analysis identified 27 significant SNPs shared between ADHD and risk behavior.

  • Longitudinal change in memory performance as a strong endophenotype for Alzheimer's disease - Unknown journal (n.d.) · Unknown authors · PubMed 37985223

    ABSTRACT: Abstract INTRODUCTION Although large‐scale genome‐wide association studies (GWAS) have been conducted on AD, few have been conducted on continuous measures of memory performance and memory decline. METHODS We conducted a cross‐ancestry GWAS on memory performance (in 27,633 participants) and memory decline (in 22,365 participants; 129,201 observations) by leveraging harmonized cognitive data from four aging cohorts. RESULTS We found high heritability for two ancestry backgrounds. Further, we found a novel ancestry locus for memory decline on chromosome 4 (rs6848524) and three loci in the non‐Hispanic Black ancestry group for memory performance on chromosomes 2 (rs111471504), 7 (rs4142249), and 15 (rs74381744). In our gene‐level analysis, we found novel genes for memory d

  • Investigating evidence for a causal association between inflammation and self-harm: A multivariable Mendelian Randomisation study - Unknown journal (n.d.) · Unknown authors · PubMed 32473944

    ABSTRACT: Highlights Observational studies of the role of inflammation on self-harm have conflicting results. We used Mendelian Randomisation, a novel causal inference technique to explore this. Genetic liability for high levels of IL-6 were not associated with self-harm. We found some evidence that higher levels of CRP were protective for self-harm. This potential protective effect of CRP has also been found for schizophrenia. Background The causal role of inflammatory markers on self-harm and suicidal risk has been studied using observational data, with conflicting results. Confounding and reverse causation can lead to bias, so we appraised question from a genetic perspective to protect against these biases. We measured associations between genetic liability for high levels of inflammato

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