| 1. |
- Jonsson, Lina, 1982, et al.
(författare)
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Association between ASMT and autistic-like traits in children from a Swedish nationwide cohort
- 2014
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Ingår i: Psychiatric Genetics. - Stockholm : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 24:1, s. 21-27
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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. |
- Lindholm, Eva, et al.
(författare)
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Reconstruction of ancestral haplotypes in a 12-generation schizophrenia pedigree
- 2004
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Ingår i: Psychiatric Genetics. - Philadelphia : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 14:1, s. 1-8
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Tidskriftsartikel (refereegranskat)abstract
- We searched for candidate chromosomal regions inherited identical by descent in 19 patients suffering from schizophrenia or schizoaffective disorder that are related 12 generations back, to an ancestral couple born in the middle of the seventeenth century. To accomplish this goal, we constructed complete chromosomal haplotypes for each patient using genotype data from 450 markers. In total, 12 haplotype regions (with sizes ranging from 0.6 to 10.9 cM) constituted by three markers each were identical in three or more of the affected individuals. The largest genomic segment was located on 6q25, a region previously shown to be significantly more frequent in patients than controls, and proposed to contain a schizophrenia susceptibility locus. For the remaining 11 candidate haplotypes, we estimated haplotype frequencies from all the 43 affected members collected from the same family and 46 unrelated control individuals. This analysis indicated that at least four of the 11 candidate haplotypes are ancestral, since the frequencies were significantly higher in patients than in controls. Five additional haplotypes showed higher estimated frequencies in the patients but the differences were not significant. Interestingly, five of these 11 genomic regions are located in, or close to, candidate regions previously suggested to contain susceptibility genes for schizophrenia. The regions are 5q21-23, 8p21-22, 1 0p13-15, 13q12-13 and 22q12-13. Several of these haplotypes are probably ancestral linkage disequilibrium blocks inherited from the original couple. There exists, however, the possibility that one or more of these regions harbour schizophrenia susceptibility loci that may have epistatic interactions among them.
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| 3. |
- Suchankova, Petra, 1979, et al.
(författare)
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The+1444C > T polymorphism in the CRP gene: a study on personality traits and suicidal behaviour
- 2013
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 23:2, s. 70-76
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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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| 4. |
- Alaerts, Maaike, et al.
(författare)
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Lack of association of an insertion/deletion polymorphism in the G protein-coupled receptor 50 with bipolar disorder in a Northern Swedish population
- 2006
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Ingår i: Psychiatric Genetics. - : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 16:6, s. 235-236
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Tidskriftsartikel (refereegranskat)abstract
- GPR50 is a G protein-coupled receptor, located on Xq28 and related to the melatonin receptor family. It is suggested as a functional and positional candidate gene for bipolar disorder (BP). Recently an insertion/deletion polymorphism in GPR50, Delta502-505, was found to be associated with BP in a Scottish association sample (P=0.007). When the analysis was restricted to female subjects, the association increased in significance (P=0.00023). We attempted to replicate this finding in a Northern Swedish association sample, but no significant association was detected (P=0.7, women only: P=0.65).
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| 5. |
- Fredrikson, Mats, et al.
(författare)
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Different genetic factors underlie fear conditioning and episodic memory
- 2015
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 25:4, s. 155-162
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Tidskriftsartikel (refereegranskat)abstract
- ObjectiveFear conditioning seems to account for the acquisition of post-traumatic stress disorder, whereas conscious recall of events in aftermath of trauma reflects episodic memory. Studies show that both fear conditioning and episodic memory are heritable, but no study has evaluated whether they reflect common or separate genetic factors. To this end, we studied episodic memory and fear conditioning in 173 healthy twin pairs using visual stimuli predicting unconditioned electric shocks.MethodsFear conditioning acquisition and extinction was determined using conditioned visual stimuli predicting unconditioned mild electric shocks, whereas electrodermal activity served as the fear learning index. Episodic memory was evaluated using cued recall of pictorial stimuli unrelated to conditioning. We used multivariate structural equation modeling to jointly analyze memory performance and acquisition as well as extinction of fear conditioning.ResultsBest-fit twin models estimated moderate genetic loadings for conditioning and memory measures, with no genetic covariation between them.ConclusionIndividual differences in fear conditioning and episodic memory reflect distinct genetically influenced processes, suggesting that the genetic risk for learning-induced anxiety disorders includes at least two memory-related genetic factors. These findings are consistent with the facts that the two separate learning forms are distant in their evolutionary development, involve different brain mechanisms, and support that genetically independent memory systems are pivotal in the development and maintenance of syndromes related to fear learning.
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| 6. |
- Van Den Bogaert, Ann, et al.
(författare)
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No allelic association or interaction of three known functional polymorphisms with bipolar disorder in a northern Swedish isolated population
- 2006
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Ingår i: Psychiatric Genetics. - : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 16:5, s. 209-212
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Tidskriftsartikel (refereegranskat)abstract
- Most genetic association studies in bipolar disorder have focussed on genes involved in major neurotransmitter systems or brain development. Functional polymorphisms in the serotonin transporter (5-HTTLPR), catechol-O-methyltransferase (Val158Met) and dopamine D3 receptor (Ser9Gly) genes have all been associated with bipolar disorder. We aimed at investigating whether these functional variants contribute to the genetic etiology of bipolar disorder in a northern Swedish isolated population. Moreover, we wanted to gain information about the synergistic contribution of these functional variants. Neither of these functional polymorphisms was associated with bipolar disorder in the northern Swedish patient-control sample nor did we find evidence of gene-gene interaction. Together, our data suggest that these functional variants are not involved in the etiology of bipolar disorder in the northern Swedish population nor did gene-gene interaction analysis support a central role of these variants in bipolar disorder.
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| 7. |
- Van Den Eede, Filip, et al.
(författare)
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Single nucleotide polymorphism analysis of corticotropin-releasing factor-binding protein gene in bipolar disorder
- 2007
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Ingår i: Psychiatric Genetics. - : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 17:5, s. 304-307
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Tidskriftsartikel (refereegranskat)abstract
- Corticotropin-releasing factor-binding protein regulates the availability of free corticotropin-releasing factor and is a functional candidate gene for affective disorders. The aim of this study was to examine the association between polymorphisms in CRF-BP gene and bipolar disorder in an isolated Swedish population. One hundred and eighty-two patients with bipolar I disorder and 333 controls from Northern Sweden were included in the study. Five single nucleotide polymorphisms and a deletion polymorphism in the CRF-BP gene were genotyped. The haplotype block structure of the gene was considered and the expectation maximization algorithm was adopted to estimate the haplotype frequencies. As a result, there were no significant associations of the different polymorphisms in the CRF-BP gene with bipolar disorder. In conclusion, this study in an isolated Swedish population does not support a role for the CRF-BP gene in the vulnerability for bipolar disorder.
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| 8. |
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| 9. |
- Wargelius, Hanna-Linn, et al.
(författare)
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Associations of MAOA-VNTR or 5HTT-LPR alleles with attention-deficit hyperactivity disorder symptoms are moderated by platelet monoamine oxidase B activity
- 2012
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 22:1, s. 42-45
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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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| 10. |
- Annerbrink, Kristina, 1974, et al.
(författare)
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Panic disorder is associated with the Val308Iso polymorphism in the hypocretin receptor gene
- 2011
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Ingår i: PSYCHIATRIC GENETICS. - : Rapid Communications of Oxford Ltd. - 0955-8829 .- 1473-5873. ; 21:2, s. 85-89
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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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