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| 2. |
- Comasco, Erika, et al.
(författare)
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Postpartum depression symptoms : a case-control study on monoaminergic functional polymorphisms and environmental stressors
- 2011
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 21:1, s. 19-28
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE:Postpartum depression (PPD) is an under diagnosed and under treated mood disorder, with negative impact on both the mother and the infant's health. The aim of this study is to examine whether genetic variations in the monoaminergic neurotransmitter system, together with environmental stressors, contribute to the development of PPD symptoms.METHODS:This nested case-control study included 275 women from a population-based cohort of delivering women in Sweden. A questionnaire containing the Edinburgh Postnatal Depression Scale was collected at 6 weeks and 6 months postpartum. Three functional polymorphisms were genotyped, catechol-O-methyltransferase (COMT)-ValMet, monoamine oxidase A (MAOA)-upstream variable number tandem repeat (uVNTR) and serotonin transporter linked polymorphic region (5HTT-LPR). Stressful life events, maternity stressors and previous psychiatric contact were considered as potential risk factors.RESULTS:COMT-ValMet was significantly associated with PPD symptoms at 6 weeks, but not at 6 months postpartum. A significant gene-gene interaction effect was present between COMT-ValMet and MAOA-uVNTR. In a gene-environment multivariate model, COMT-ValMet, psychiatric contact and maternity stressors were significantly associated with PPD symptoms. Among those with history of psychiatric problems, the COMT-ValMet and 5HTT-LPR risk variants were associated with PPD symptoms, whereas in the absence of previous psychiatric contact only maternity stressors were related to PPD symptoms.CONCLUSION:The interaction effect between monoaminergic genes and environmental stressors is likely to contribute to vulnerability for PPD. The different patterns of association according to history of psychiatric problems, if replicated, might be helpful in screening strategies.
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| 3. |
- DeYoung, Colin G., et al.
(författare)
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Variation in the catechol-O-methyltransferase Val(158)Met polymorphism associated with conduct disorder and ADHD symptoms, among adolescent male delinquents
- 2010
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 20:1, s. 20-24
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Tidskriftsartikel (refereegranskat)abstract
- Objective Variation in the catechol-O-methyltransferase gene (COMT) has been associated with antisocial behavior in populations with attention deficit/hyperactivity disorder (ADHD). This study examined whether COMT would predict antisocial behavior in a sample with high levels of behavior problems, not necessarily ADHD. In addition, because previous research suggests that COMT may be associated with ADHD in males, association between COMT and ADHD symptoms was examined. Method This study tested whether variation in three polymorphisms of the COMT gene was predictive of symptoms of conduct disorder and ADHD, in a sample of 174 incarcerated Russian adolescent male delinquents. Results The Val allele of the Val(158)Met polymorphism was significantly associated with conduct disorder diagnosis and symptoms, whereas the Met allele was associated with ADHD symptoms. Conclusion The Val(158)Met polymorphism of the COMT gene shows a complex relation to behavior problems, influencing conduct disorder and ADHD symptoms in opposite directions in a high-risk population. Psychiatr Genet 20:20-24 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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| 4. |
- 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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| 5. |
- Hiio, Kelli, et al.
(författare)
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Effects of serotonin transporter promoter and BDNF Val66Met genotype on personality traits in a population representative sample of adolescents
- 2011
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 21:5, s. 261-264
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of this study was to investigate the effects of the 5-HTTLPR and brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms on self-reported Big Five personality traits and their facets in a population representative sample of adolescents. The sample consisted of both cohorts of the Estonian Children Personality Behaviour and Health Study, and personality data were collected during its second waves. The 5-HTTLPR and BDNF Val66Met polymorphisms were genotyped. The BDNF Val66Met had a significant effect on conscientiousness [F(1,807) = 4.32, P = 0.038]. We did not find effects of the 5-HTTLPR polymorphism on the main domains of personality, however, a gene x gene interaction on conscientiousness emerged -BDNF Val66Met Met-allele carriers with the 5-HTTLPR s/s genotype had by far the lowest scores in conscientiousness [F(2,803) = 4.38, P = 0.012]. In addition, we found genotype effects on some facet scales. In conclusion, the BDNF Val66Met genotype Met-allele carriers have lower conscientiousness, and this effect is increased in the 5-HTTLPR s/s individuals.
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| 6. |
- 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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| 7. |
- Squassina, Alessio, et al.
(författare)
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Zinc finger proteins in psychiatric disorders and response to psychotropic medications
- 2019
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 29:5, s. 132-141
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Forskningsöversikt (refereegranskat)abstract
- Zinc finger proteins are a large family of abundantly expressed small motifs that play a crucial role in a wide range of physiological and pathophysiological mechanisms. Findings published so far support an involvement of zinc fingers in psychiatric disorders. Most of the evidence has been provided for the zinc finger protein 804A (ZNF804A) gene, which has been suggested to be implicated in schizophrenia and bipolar disorder. This evidence has been corroborated by a wide range of functional studies showing that ZNF804A regulates the expression of genes involved in cell adhesion and plays a crucial role in neurite formation and maintenance of dendritic spines. On the other hand, far less is known on other zinc finger proteins and their involvement in psychiatric disorders. In this review, we discussed studies exploring the role of zinc finger proteins in schizophrenia, bipolar disorder, and major depressive disorder as well as in pharmacogenetics of psychotropic drugs.
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| 8. |
- Visscher, Peter M., et al.
(författare)
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Genetic survival analysis of age-at-onset of bipolar disorder : evidence for anticipation or cohort effect in families
- 2001
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Ingår i: Psychiatric Genetics. - : Lippincott Williams & Wilkins. - 0955-8829 .- 1473-5873. ; 11:3, s. 129-137
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Tidskriftsartikel (refereegranskat)abstract
- Age-at-onset (AAO) in a number of extended families ascertained for bipolar disorder was analysed using survival analysis techniques, fitting proportional hazards models to estimate the fixed effects of sex, year of birth, and generation, and a random polygenic genetic effect. Data comprised the AAO (for 171 affecteds) or age when last seen (ALS) for 327 unaffecteds, on 498 individuals in 27 families. ALS was treated as the censored time in the statistical analyses. The majority of individuals classified as affected were diagnosed with bipolar I and II (n = 103) or recurrent major depressive disorder (n = 68). In addition to the significant effects of sex and year of birth, a fitted ‘generation’ effect was highly significant, which could be interpreted as evidence for an anticipation effect. The risk of developing bipolar or unipolar disorder increased twofold with each generation descended from the oldest founder. However, although information from both affected and unaffected individuals was used to estimate the relative risk of subsequent generations, it is possible that the results are biased because of the ‘Penrose effect’. Females had a twofold increased risk in developing depressive disorder relative to males. The risk of developing bipolar or unipolar disorder increased by approximately 4% per year of birth. A polygenic component of variance was estimated, resulting in a ‘heritability’ of AAO of approximately 0.52. In a family showing strong evidence of linkage to chromosome 4p (family 22), the ‘affected haplotype’ increased the relative risk of being affected by a factor of 46. In this family, there was strong evidence of a time trend in the AAO. When either year of birth or generation was fitted in the model, these effects were highly significant, but neither was significant in the presence of the other. For this family, there was no increase in trinucleotide repeats measured by the repeat expansion detection method in affected individuals compared with control subjects. Proportional hazard models appear appropriate to analyse AAO data, and the methodology will be extended to map quantitative trait loci (QTL) for AAO.
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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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