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Sökning: (L773:0955 8829 OR L773:1473 5873) hsvcat:3 > (2010-2014)

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1.
  • Jonsson, Lina, 1982, et al. (författare)
  • Association between ASMT and autistic-like traits in children from a Swedish nationwide cohort
  • 2014
  • Ingår i: Psychiatric Genetics. - Stockholm : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 24:1, s. 21-27
  • Tidskriftsartikel (refereegranskat)abstract
    • Individuals with autism spectrum disorders often show low levels of melatonin, and it has been suggested that this decrease may be because of the low activity of the acetylserotonin O-methyltransferase (ASMT), the last enzyme in the melatonin-synthesis pathway. Also, genetic variants in ASMT have been associated with autism, as well as with low ASMT activity and melatonin levels, suggesting that the low ASMT activity observed in autism may partly be because of variations within the ASMT gene. In this study, we present a symptom-based approach to investigate possible associations between ASMT and autistic-like traits in the general population. To this end, continuous measures of autistic-like traits were assessed in a nationally representative twin cohort (n=1771) from Sweden and six single nucleotide polymorphisms (SNPs), and a duplication of exons 2-8 in ASMT were genotyped. Our results show a nominally significant association, in girls, between one single nucleotide polymorphism (rs5949028) in the last intron of ASMT and social interaction impairments. No significant association, however, was observed with traits related to language impairment or restricted and repetitive behavior. In conclusion, our results support the possible involvement of the ASMT gene in autism spectrum disorders, and our finding that only one of the three traits shows association suggests that genetic research may benefit from adopting a symptom-specific approach to identify genes involved in autism psychopathology.
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2.
  • Suchankova, Petra, 1979, et al. (författare)
  • The+1444C > T polymorphism in the CRP gene: a study on personality traits and suicidal behaviour
  • 2013
  • Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 23:2, s. 70-76
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Numerous studies have shown associations between an on-going depression and elevated serum levels of the acute-phase reactant C-reactive protein (CRP). Also, in suicidal behaviour, a proinflammatory state has been suggested to be of importance for the pathophysiology. There is a genetic susceptibility to suicidal behaviour, but studies with respect to genes related to inflammation are sparse. We have previously reported an association between a polymorphism located in the CRP gene, +1444C>T (rs1130864), and the personality trait impulsiveness in women assessed using the Karolinska Scales of Personality. The present study aims to replicate these results in suicide attempters and examine whether the polymorphism is associated with suicidal behaviour. Materials and methods: The +1444C>T polymorphism was genotyped in suicide attempters from two cohorts (a total of 106 patients) and healthy controls (n=517). Results: We could replicate our previous finding, as the +1444T allele was associated with higher scores in the Karolinska Scales of Personality factor extraversion and its subscale impulsiveness in one of the patient cohorts. Furthermore, the +1444T allele was significantly more common among suicide attempters compared with the +1444C allele. Conclusion: The present results lend further support to the relevance of inflammation for suicidal behaviour. The association between the polymorphism and personality trait impulsiveness reinforces our hypothesis of the importance of immune-related genes also for normal mental functions such as personality traits. Given the fact that impulsiveness is a well-known risk factor for suicidal behaviour, we further hypothesize that the polymorphism studied may in part explain this relationship.
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3.
  • Wargelius, Hanna-Linn, et al. (författare)
  • Associations of MAOA-VNTR or 5HTT-LPR alleles with attention-deficit hyperactivity disorder symptoms are moderated by platelet monoamine oxidase B activity
  • 2012
  • Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 22:1, s. 42-45
  • Tidskriftsartikel (refereegranskat)abstract
    • The monoamine systems have been suggested to play a role in the biological basis of ADHD symptoms. Thus, polymorphisms in e.g. the monoamine oxidase A (MAOA) and the serotonin transporter (5HTT) genes have been associated with ADHD like phenotypes. Furthermore, platelet MAOB activity has frequently been linked to impulsiveness-related traits. In the present paper, we have studied ADHD symptoms with regard to the combination of platelet MAOB activity and MAOAVNTR or 5HTT-LPR genotype. The study group consisted of 156 adolescent twin pairs, i.e. 312 individuals, who were used in a previous study (Malmberg et al., 2008). ADHD symptoms were scored with a structured clinical interview of both the twin and a parent using Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version. Presence of a short 5HTT-LPR or short MAOA-VNTR allele, in combination with high levels of platelet MAOB enzyme activity was associated with higher scores of ADHD like problems (p<0.001; p<0.01, respectively). This reexamination of ADHD scores in a non-clinical sample suggests that effects of the MAOA-VNTR and 5HTT-LPR are moderated by platelet MAOB activity.  
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4.
  • Annerbrink, Kristina, 1974, et al. (författare)
  • Panic disorder is associated with the Val308Iso polymorphism in the hypocretin receptor gene
  • 2011
  • Ingår i: PSYCHIATRIC GENETICS. - : Rapid Communications of Oxford Ltd. - 0955-8829 .- 1473-5873. ; 21:2, s. 85-89
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Orexin A and B are neuropeptides influencing, for example, arousal and respiration. Although panic disorder is characterized by both enhanced proneness for arousal and by respiratory abnormalities, the possible influence of orexin-related genes on the risk of developing this disorder has not been studied until now. Methods We have analyzed the Ile408Val polymorphism in the hypocretin receptor 1 (HCRTR1) gene and the Val308Iso (G1246A) polymorphism in the hypocretin receptor 2 (HCRTR2) gene in a sample of 215 panic disorder patients and 454 controls. Results Although the polymorphism in the HCRTR1 did not differ between groups, the Iso allele of the HCRTR2 polymorphism was significantly more frequent in patients than in controls. After the population was divided according to sex, the association between the Iso allele of the Val308Iso polymorphism and panic disorder was observed only in female patients. Conclusion Our results suggest that the HCRTR2 polymorphism may be of importance for the pathophysiology of panic disorder. The results should be regarded as preliminary until replicated in an independent sample. This indicates that further research on the possible role of orexin in panic disorder may prove rewarding.
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5.
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6.
  • Van Schijndel, Jessica E., et al. (författare)
  • Dual association of a TRKA polymorphism with schizophrenia
  • 2011
  • Ingår i: Psychiatric Genetics. - : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 21:3, s. 125-131
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: An interaction between predisposing genes and environmental stressors is thought to underlie the neurodevelopmental disorder schizophrenia. In a targeted gene screening, we previously found that the minor allele of the single nucleotide polymorphism (SNP) rs6336 in the neurotrophic tyrosine kinase receptor 1 (NTRK1/TRKA) gene is associated with schizophrenia as a risk factor.METHODS: We genotyped the TRKA SNP in a total of eight independent Caucasian schizophrenia case-control groups.RESULT: Remarkably, although in five of the groups a higher frequency of the risk allele was indeed found in the patients compared with the controls, in the three other groups the SNP acted as a protective factor.CONCLUSION: An intriguing possibility is that this dual character of the TRKA SNP is caused by its interaction with endophenotypic and/or epistatic factors.
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