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Sökning: WFRF:(Danner U)

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1.
  • Munn-Chernoff, M. A., et al. (författare)
  • Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies
  • 2021
  • Ingår i: Addiction Biology. - 1355-6215 .- 1369-1600. ; 26:1, s. e12880-
  • Tidskriftsartikel (refereegranskat)abstract
    • Eating disorders and substance use disorders frequently co-occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [r(g)], twin-based = 0.23-0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome-wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance-use-related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from similar to 2400 to similar to 537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism-based genetic correlations between eating disorder- and substance-use-related phenotypes. Significant positive genetic associations emerged between AUD and AN (r(g) = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (r(g) = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (r(g) = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating (r(gs) = -0.19 to -0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co-varying for major depressive disorder loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships among these behaviors.
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  • Watson, H. J., et al. (författare)
  • Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa
  • 2019
  • Ingår i: Nature Genetics. - 1061-4036 .- 1546-1718. ; 51:8, s. 1207-
  • Tidskriftsartikel (refereegranskat)abstract
    • Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness(1), affecting 0.9-4% of women and 0.3% of men(2-4), with twin-based heritability estimates of 50-60%(5). Mortality rates are higher than those in other psychiatric disorders(6), and outcomes are unacceptably poor(7). Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)(8,9) and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes.
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  • Bryois, J., et al. (författare)
  • Genetic identification of cell types underlying brain complex traits yields insights into the etiology of Parkinson’s disease
  • 2020
  • Ingår i: Nature Genetics. - 1061-4036. ; 52:5, s. 482-493
  • Tidskriftsartikel (refereegranskat)abstract
    • Genome-wide association studies have discovered hundreds of loci associated with complex brain disorders, but it remains unclear in which cell types these loci are active. Here we integrate genome-wide association study results with single-cell transcriptomic data from the entire mouse nervous system to systematically identify cell types underlying brain complex traits. We show that psychiatric disorders are predominantly associated with projecting excitatory and inhibitory neurons. Neurological diseases were associated with different cell types, which is consistent with other lines of evidence. Notably, Parkinson’s disease was genetically associated not only with cholinergic and monoaminergic neurons (which include dopaminergic neurons) but also with enteric neurons and oligodendrocytes. Using post-mortem brain transcriptomic data, we confirmed alterations in these cells, even at the earliest stages of disease progression. Our study provides an important framework for understanding the cellular basis of complex brain maladies, and reveals an unexpected role of oligodendrocytes in Parkinson’s disease. © 2020, The Author(s), under exclusive licence to Springer Nature America, Inc.
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  • Coumans, J. M. J., et al. (författare)
  • Emotion-driven impulsiveness and snack food consumption of European adolescents: Results from the I.Family study
  • 2018
  • Ingår i: Appetite. - 0195-6663 .- 1095-8304. ; 123, s. 152-159
  • Tidskriftsartikel (refereegranskat)abstract
    • We aimed to investigate the association between emotion-driven impulsiveness and snack food consumption in 1039 European adolescents aged 12–18 years. During the cross-sectional examination in 2013/2014, complete information was collected on: emotion-driven impulsiveness (using the negative urgency subscale from the Urgency, Premeditation, Perseverance, Sensation seeking, and Positive urgency (UPPS-P) Impulsive Behaviour Scale) and snacking behaviour operationalised as 1) consumption frequency of daily snacks, 2) consumption frequency of energy-dense snacks (both measured using Food Frequency Questionnaire) and 3) usual energy intake of food consumed per snacking occasion in calories. The latter was measured using online self-administered 24-h dietary recalls and was estimated based on the National Cancer Institute (NCI) Method. Anthropometric variables were measured and BMI z-score (zBMI) calculated. Age, sex, highest education level of the family and country of residence were assessed using a questionnaire. Mixed-effect regression analyses were separately conducted for each snacking behaviour outcome with emotion-driven impulsiveness as the exposure. After controlling for zBMI, age, sex, country and socioeconomic status, emotion-driven impulsiveness was positively associated with daily consumption frequency of snacks (β = 0.07, 95% Confidence Interval (CI) [0.02, 0.12]) and consumption frequency of energy-dense snacks (β = 0.25, 95% CI [0.19, 0.31]), but not with usual energy intake of food per snacking (β = 2.52, 95% CI [-0.55, 5.59]). Adolescents with a stronger emotion-driven impulsiveness tendency reported a higher snacking frequency and specifically more energy-dense snacks, whereas the energy intake of snack food seemed less important. These findings have implications for obesity prevention and treatment as they indicate the importance of targeting emotion-driven impulsiveness as a strategy to avoid excessive snacking.
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