SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:1476 5578 "

Sökning: L773:1476 5578

Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
21.
  •  
22.
  •  
23.
  • Borg, J., et al. (författare)
  • Contribution of non-genetic factors to dopamine and serotonin receptor availability in the adult human brain
  • 2016
  • Ingår i: Molecular Psychiatry. - London, United Kingdom : NATURE PUBLISHING GROUP. - 1359-4184 .- 1476-5578. ; 51, s. 879-879
  • Tidskriftsartikel (refereegranskat)abstract
    • The dopamine (DA) and serotonin (5-HT) neurotransmission systems are of fundamental importance for normal brain function and serve as targets for treatment of major neuropsychiatric disorders. Despite central interest for these neurotransmission systems in psychiatry research, little is known about the regulation of receptor and transporter density levels. This lack of knowledge obscures interpretation of differences in protein availability reported in psychiatric patients. In this study, we used positron emission tomography (PET) in a twin design to estimate the relative contribution of genetic and environmental factors, respectively, on dopaminergic and serotonergic markers in the living human brain. Eleven monozygotic and 10 dizygotic healthy male twin pairs were examined with PET and [C-11]raclopride binding to the D-2- and D-3-dopamine receptor and [C-11]WAY100635 binding to the serotonin 5-HT1A receptor. Heritability, shared environmental effects and individual-specific non-shared effects were estimated for regional D-2/3 and 5-HT1A receptor availability in projection areas. We found a major contribution of genetic factors (0.67) on individual variability in striatal D-2/3 receptor binding and a major contribution of environmental factors (pairwise shared and unique individual; 0.70-0.75) on neocortical 5-HT1A receptor binding. Our findings indicate that individual variation in neuroreceptor availability in the adult brain is the end point of a nature-nurture interplay, and call for increased efforts to identify not only the genetic but also the environmental factors that influence neurotransmission in health and disease.
  •  
24.
  • Brander, Gustaf, et al. (författare)
  • A population-based family clustering study of tic-related obsessive-compulsive disorder
  • 2021
  • Ingår i: Molecular Psychiatry. - : Nature Publishing Group. - 1359-4184 .- 1476-5578. ; 26:4, s. 1224-1233
  • Tidskriftsartikel (refereegranskat)abstract
    • In the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), obsessive-compulsive disorder (OCD) included a new "tic-related" specifier. However, strong evidence supporting tic-related OCD as a distinct subtype of OCD is lacking. This study investigated whether, at the population level, tic-related OCD has a stronger familial load than non-tic-related OCD. From a cohort of individuals born in Sweden between 1967 and 2007 (n = 4,085,367; 1257 with tic-related OCD and 20,975 with non-tic-related OCD), we identified all twins, full siblings, maternal and paternal half siblings, and cousins. Sex- and birth year-adjusted hazard ratios (aHR) were calculated to estimate the risk of OCD in relatives of individuals with OCD with and without comorbid tics, compared with relatives of unaffected individuals. We found that OCD is a familial disorder, regardless of comorbid tic disorder status. However, the risk of OCD in relatives of individuals with tic-related OCD was considerably greater than the risk of OCD in relatives of individuals with non-tic-related OCD (e.g., risk for full siblings: aHR = 10.63 [95% CI, 7.92-14.27] and aHR = 4.52 [95% CI, 4.06-5.02], respectively; p value for the difference < 0.0001). These differences remained when the groups were matched by age at first OCD diagnosis and after various sensitivity analyses. The observed familial patterns of OCD in relation to tics were not seen in relation to other neuropsychiatric comorbidities. Tic-related OCD is a particularly familial subtype of OCD. The results have important implications for ongoing gene-searching efforts.
  •  
25.
  • Brander, Gustaf, et al. (författare)
  • Perinatal risk factors in Tourette's and chronic tic disorders : a total population sibling comparison study
  • 2018
  • Ingår i: Molecular Psychiatry. - : Nature Publishing Group. - 1359-4184 .- 1476-5578. ; 23:5, s. 1189-1197
  • Tidskriftsartikel (refereegranskat)abstract
    • Adverse perinatal events may increase the risk of Tourette's and chronic tic disorders (TD/CTD), but previous studies have been unable to control for unmeasured environmental and genetic confounding. We aimed to prospectively investigate potential perinatal risk factors for TD/CTD, taking unmeasured factors shared between full siblings into account. A population-based birth cohort, consisting of all singletons born in Sweden in 1973-2003, was followed until December 2013. A total of 3 026 861 individuals were identified, 5597 of which had a registered TD/CTD diagnosis. We then studied differentially exposed full siblings from 947 942 families; of these, 3563 families included siblings that were discordant for TD/CTD. Perinatal data were collected from the Medical Birth Register and TD/CTD diagnoses were collected from the National Patient Register, using a previously validated algorithm. In the fully adjusted models, impaired fetal growth, preterm birth, breech presentation and cesarean section were associated with a higher risk of TD/CTD, largely independent from shared family confounders and measured covariates. Maternal smoking during pregnancy was associated with risk of TD/CTD in a dose-response manner but the association was no longer statistically significant in the sibling comparison models or after the exclusion of comorbid attention-deficit/hyperactivity disorder. A dose-response relationship between the number of adverse perinatal events and increased risk for TD/CTD was also observed, with hazard ratios ranging from 1.41 (95% confidence interval (CI): 1.33-1.50) for one event to 2.42 (95% CI: 1.65-3.53) for five or more events. These results pave the way for future gene by environment interaction and epigenetic studies in TD/CTD.
  •  
26.
  • Brikell, Isabell, et al. (författare)
  • The contribution of common genetic risk variants for ADHD to a general factor of childhood psychopathology
  • 2020
  • Ingår i: Molecular Psychiatry. - : Nature Publishing Group. - 1359-4184 .- 1476-5578. ; 25:8, s. 1809-1821
  • Tidskriftsartikel (refereegranskat)abstract
    • Common genetic risk variants have been implicated in the etiology of clinical attention-deficit/hyperactivity disorder (ADHD) diagnoses and symptoms in the general population. However, given the extensive comorbidity across ADHD and other psychiatric conditions, the extent to which genetic variants associated with ADHD also influence broader psychopathology dimensions remains unclear. The aim of this study was to evaluate the associations between ADHD polygenic risk scores (PRS) and a broad range of childhood psychiatric symptoms, and to quantify the extent to which such associations can be attributed to a general factor of childhood psychopathology. We derived ADHD PRS for 13,457 children aged 9 or 12 from the Child and Adolescent Twin Study in Sweden, using results from an independent meta-analysis of genome-wide association studies of ADHD diagnosis and symptoms. We estimated associations between ADHD PRS, a general psychopathology factor, and several dimensions of neurodevelopmental, externalizing, and internalizing symptoms, using structural equation modeling. Higher ADHD PRS were statistically significantly associated with elevated neurodevelopmental, externalizing, and depressive symptoms (R 2  = 0.26-1.69%), but not with anxiety. After accounting for a general psychopathology factor, on which all symptoms loaded positively (mean loading = 0.50, range = 0.09-0.91), an association with specific hyperactivity/impulsivity remained significant. ADHD PRS explained ~ 1% (p value < 0.0001) of the variance in the general psychopathology factor and ~ 0.50% (p value < 0.0001) in specific hyperactivity/impulsivity. Our results suggest that common genetic risk variants associated with ADHD, and captured by PRS, also influence a general genetic liability towards broad childhood psychopathology in the general population, in addition to a specific association with hyperactivity/impulsivity symptoms.
  •  
27.
  •  
28.
  •  
29.
  •  
30.
  •  
Skapa referenser, mejla, bekava och länka
Typ av publikation
tidskriftsartikel (274)
forskningsöversikt (6)
konferensbidrag (1)
Typ av innehåll
refereegranskat (256)
övrigt vetenskapligt (25)
Författare/redaktör
Sullivan, PF (37)
Landén, Mikael, 1966 (23)
Lichtenstein, P (17)
Larsson, Henrik, 197 ... (16)
Sklar, P (16)
Cichon, S. (16)
visa fler...
Rietschel, M (15)
O'Donovan, MC (15)
Owen, MJ (13)
Ripke, S (12)
Andreassen, OA (11)
Breen, G (11)
Corvin, A (11)
Rujescu, D (11)
Mattheisen, M (11)
Djurovic, S (10)
Stefansson, H. (10)
Wang, Y. (9)
Svenningsson, P (9)
Agartz, I (9)
Bulik, CM (9)
Boomsma, DI (9)
Zetterberg, Henrik, ... (9)
Craddock, N (9)
Gill, M. (9)
Hottenga, JJ (8)
Willemsen, G (8)
Kirov, G (8)
Muller-Myhsok, B (8)
Hultman, C (8)
Metspalu, A (8)
Leboyer, M. (8)
Kuja-Halkola, Ralf (8)
Mataix-Cols, David (8)
Nothen, MM (8)
Stefansson, K. (8)
Steinberg, S (7)
Penninx, BWJH (7)
Werge, T (7)
Crowley, JJ (7)
Hoffmann, P (7)
Jonsson, EG (7)
Milaneschi, Y. (7)
Palotie, A (7)
Kuja-Halkola, R. (7)
Lichtenstein, Paul (7)
Schalling, M (7)
Cervenka, Simon (7)
Rück, Christian (7)
Hultman, C. M. (7)
visa färre...
Lärosäte
Karolinska Institutet (221)
Göteborgs universitet (45)
Uppsala universitet (37)
Örebro universitet (19)
Umeå universitet (13)
Linköpings universitet (11)
visa fler...
Stockholms universitet (8)
Lunds universitet (8)
Kungliga Tekniska Högskolan (3)
Mittuniversitetet (3)
Chalmers tekniska högskola (3)
Mälardalens universitet (1)
Högskolan i Skövde (1)
Södertörns högskola (1)
Linnéuniversitetet (1)
visa färre...
Språk
Engelska (281)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (111)
Naturvetenskap (18)
Samhällsvetenskap (6)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy