SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Alfredsson L) "

Sökning: WFRF:(Alfredsson L)

Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
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.
  •  
2.
  • 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.
  •  
3.
  • 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.
  •  
4.
  •  
5.
  • Beecham, Ashley H, et al. (författare)
  • Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis.
  • 2013
  • Ingår i: Nature genetics. - : NATURE PUBLISHING GROUP, 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA. - 1546-1718 .- 1061-4036. ; 45:11, s. 1353-60
  • Tidskriftsartikel (refereegranskat)abstract
    • Using the ImmunoChip custom genotyping array, we analyzed 14,498 subjects with multiple sclerosis and 24,091 healthy controls for 161,311 autosomal variants and identified 135 potentially associated regions (P < 1.0 × 10(-4)). In a replication phase, we combined these data with previous genome-wide association study (GWAS) data from an independent 14,802 subjects with multiple sclerosis and 26,703 healthy controls. In these 80,094 individuals of European ancestry, we identified 48 new susceptibility variants (P < 5.0 × 10(-8)), 3 of which we found after conditioning on previously identified variants. Thus, there are now 110 established multiple sclerosis risk variants at 103 discrete loci outside of the major histocompatibility complex. With high-resolution Bayesian fine mapping, we identified five regions where one variant accounted for more than 50% of the posterior probability of association. This study enhances the catalog of multiple sclerosis risk variants and illustrates the value of fine mapping in the resolution of GWAS signals.
  •  
6.
  •  
7.
  • Madsen, I. E. H., et al. (författare)
  • Study protocol for examining job strain as a risk factor for severe unipolar depression in an individual participant meta-analysis of 14 European cohorts
  • 2014
  • Ingår i: F1000Research. - 2046-1402. ; 2, s. Art. no. 2-233.v2-
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Previous studies have shown that gainfully employed individuals with high work demands and low control at work (denoted "job strain?) are at increased risk of common mental disorders, including depression. Most existing studies have, however, measured depression using self-rated symptom scales that do not necessarily correspond to clinically diagnosed depression. In addition, a meta-analysis from 2008 indicated publication bias in the field. Methods: This study protocol describes the planned design and analyses of an individual participant data meta-analysis, to examine whether job strain is associated with an increased risk of clinically diagnosed unipolar depression based on hospital treatment registers. The study will be based on data from approximately 120,000 individuals who participated in 14 studies on work environment and health in 4 European countries. The self-reported working conditions data will be merged with national registers on psychiatric hospital treatment, primarily hospital admissions. Study-specific risk estimates for the association between job strain and depression will be calculated using Cox regressions. The study-specific risk estimates will be pooled using random effects meta-analysis. Discussion: The planned analyses will help clarify whether job strain is associated with an increased risk of clinically diagnosed unipolar depression. As the analysis is based on pre-planned study protocols and an individual participant data meta-analysis, the pooled risk estimates will not be influenced by selective reporting and publication bias. However, the results of the planned study may only pertain to severe cases of unipolar depression, because of the outcome measure applied.
  •  
8.
  •  
9.
  • Sawcer, Stephen, et al. (författare)
  • Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis
  • 2011
  • Ingår i: Nature. - 0028-0836 .- 1476-4687. ; 476:7359, s. 214-219
  • Tidskriftsartikel (refereegranskat)abstract
    • Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
Typ av publikation
tidskriftsartikel (515)
konferensbidrag (89)
forskningsöversikt (7)
doktorsavhandling (2)
bokkapitel (1)
annan publikation (1)
visa fler...
visa färre...
Typ av innehåll
refereegranskat (486)
övrigt vetenskapligt (128)
populärvet., debatt m.m. (1)
Författare/redaktör
Alfredsson, L (600)
KLARESKOG, L (195)
Alfredsson, Lars (168)
Olsson, T. (141)
Padyukov, L (120)
Kockum, I. (90)
visa fler...
Hillert, J (80)
Knutsson, A. (69)
Theorell, T (62)
Knutsson, Anders (58)
Batty, G. David (58)
Nyberg, Solja T (56)
Hedstrom, AK (55)
Bengtsson, C (54)
Nordin, M. (52)
Fransson, Eleonor I (52)
Kallberg, H (52)
Westerlund, H (51)
Vahtera, J (48)
Singh-Manoux, A (47)
Pentti, J (45)
Theorell, Töres (44)
Nordin, Maria (43)
Ferrie, Jane E (43)
Virtanen, M (42)
Kivimaki, M (40)
Saevarsdottir, S (40)
Koskenvuo, M (40)
Westerlund, Hugo (40)
Madsen, Ida E. H. (40)
Klareskog, Lars (39)
Oksanen, T (39)
Rugulies, R (39)
Nielsen, Martin L (38)
Kivimäki, Mika (37)
Westerholm, P (37)
Singh-Manoux, Archan ... (36)
Westerholm, Peter J ... (36)
Nyberg, ST (36)
Vahtera, Jussi (35)
Bjorner, Jakob B (35)
Pentti, Jaana (34)
Ding, B (34)
Batty, GD (34)
Fransson, EI (34)
Dragano, N (34)
Westerholm, Peter (33)
Burr, H. (33)
Virtanen, Marianna (32)
Vingard, E (32)
visa färre...
Lärosäte
Karolinska Institutet (468)
Uppsala universitet (79)
Lunds universitet (41)
Stockholms universitet (41)
Umeå universitet (38)
Mittuniversitetet (34)
visa fler...
Jönköping University (29)
Göteborgs universitet (20)
Kungliga Tekniska Högskolan (20)
Linköpings universitet (18)
Högskolan i Skövde (17)
Örebro universitet (11)
Mälardalens högskola (3)
Högskolan i Borås (3)
Högskolan Dalarna (3)
Högskolan i Halmstad (2)
Södertörns högskola (1)
Högskolan i Gävle (1)
RISE (1)
Sveriges Lantbruksuniversitet (1)
visa färre...
Språk
Engelska (613)
Svenska (1)
Odefinierat språk (1)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (174)
Naturvetenskap (13)
Samhällsvetenskap (12)
Teknik (10)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy