| 1. |
- Walum, Hasse, et al.
(författare)
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Genetic variation in the vasopressin receptor 1a gene (AVPR1A) associates with pair-bonding behavior in humans.
- 2008
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 105:37, s. 14153-14156
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Tidskriftsartikel (refereegranskat)abstract
- Pair-bonding has been suggested to be a critical factor in the evolutionary development of the social brain. The brain neuropeptide arginine vasopressin (AVP) exerts an important influence on pair-bonding behavior in voles. There is a strong association between a polymorphic repeat sequence in the 5' flanking region of the gene (avpr1a) encoding one of the AVP receptor subtypes (V1aR), and proneness for monogamous behavior in males of this species. It is not yet known whether similar mechanisms are important also for human pair-bonding. Here, we report an association between one of the human AVPR1A repeat polymorphisms (RS3) and traits reflecting pair-bonding behavior in men, including partner bonding, perceived marital problems, and marital status, and show that the RS3 genotype of the males also affects marital quality as perceived by their spouses. These results suggest an association between a single gene and pair-bonding behavior in humans, and indicate that the well characterized influence of AVP on pair-bonding in voles may be of relevance also for humans.
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| 2. |
- Wirdefeldt, Karin, et al.
(författare)
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Complete ascertainment of Parkinson disease in the Swedish Twin Registry
- 2008
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Ingår i: Neurobiology of Aging. - : Elsevier BV. - 1558-1497 .- 0197-4580. ; 29:12, s. 1765-1773
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Tidskriftsartikel (refereegranskat)abstract
- This report describes the ascertainment of Parkinson disease (PD) in all individuals aged 50 years or older (49,814 individuals) from the Swedish Twin Registry. In phase one of the study, all twins were screened for PD using telephone interviews, with a response rate of 72.7%. In phase two, twins with suspected PD were re-contacted to exclude anyone from follow-up who reported parkinsonian symptoms due to diseases other than PD. In the third phase, in-person clinical evaluations were completed for twins who were still considered PD suspects after phase two and for a sample of co-twins. During the clinical evaluations, we also collected blood samples and information about a variety of environmental exposures. Overall prevalence rate for PD was 496 per 100,000 individuals. Among the 132 PD cases identified, there were only three concordant twin pairs. In total 7.2% of PD cases reported a first degree relative with PD.
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| 3. |
- Yuh, Jongil, et al.
(författare)
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The role of temperament and social support in depressive symptoms: A twin study of mid-aged women
- 2008
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Ingår i: Journal of Affective Disorders. - : Elsevier BV. - 1573-2517 .- 0165-0327. ; 106:1-2, s. 99-105
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Tidskriftsartikel (refereegranskat)abstract
- Background: Although research has found that temperament and social support are associated with depression, these relationships have not been explored in conjunction with one another as they relate to depression using a genetically informative design. This study investigated how the association among the three constructs is mediated. Methods: The sample in this study consisted of 326 pairs of adult monozygotic and dizygotic twins drawn from the Swedish Twin Registry. Twins were mothers of adolescent from married or partnered relationships. The genetic and environmental contributions to the association were evaluated by self-reported measures of temperament, social support, and depressive symptoms. Results: Multivariate genetic model fitting revealed that a moderate portion of genetic influences were common among the three central constructs of harm avoidance, perceived social support, and depressive symptoms. Limitations: The results may not be generalizable to depressive disorders in clinical settings. The measures were self-reported from a cross-sectional study. Conclusions: The findings suggest that the heritable component may contribute to genetic influences on an individual's ability to secure social support and thus to genetic risk for depressive symptomatology in women.
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| 4. |
- Kato, K, et al.
(författare)
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A population-based twin study of functional somatic syndromes
- 2009
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Ingår i: Psychological Medicine. - : Cambridge University Press. - 0033-2917 .- 1469-8978. ; 39:3, s. 497-505
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The mechanisms underlying the co-occurrence of the functional somatic syndromes are largely unknown. No empirical study has explicitly examined how genetic and environmental factors influence the co-morbidity of these syndromes. We aimed to examine how the co-morbidity of functional somatic syndromes is influenced by genetic and environmental factors that are in common to the syndromes. METHOD: A total of 31318 twins in the Swedish Twin Registry aged 41-64 years underwent screening interviews via a computer-assisted telephone system from 1998 to 2002. Four functional somatic syndromes (chronic widespread pain, chronic fatigue, irritable bowel syndrome, and recurrent headache) and two psychiatric disorders (major depression and generalized anxiety disorder) were assessed using structured questions based on standard criteria for each illness in a blinded manner. RESULTS: Multivariate twin analyses revealed that a common pathway model with two latent traits that were shared by the six illnesses fit best to the women's data. One of the two latent traits loaded heavily on the psychiatric disorders, whereas the other trait loaded on all four of the functional somatic syndromes, particularly chronic widespread pain, but not on the psychiatric disorders. All illnesses except the psychiatric disorders were also affected by genetic influences that were specific to each. CONCLUSIONS: The co-occurrence of functional somatic syndromes in women can be best explained by affective and sensory components in common to all these syndromes, as well as by unique influences specific to each of them. The findings clearly suggest a complex view of the multifactorial pathogenesis of these illnesses.
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| 5. |
- Åberg, Maria A I, 1972, et al.
(författare)
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Cardiovascular fitness is associated with cognition in young adulthood.
- 2009
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490.
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Tidskriftsartikel (refereegranskat)abstract
- During early adulthood, a phase in which the central nervous system displays considerable plasticity and in which important cognitive traits are shaped, the effects of exercise on cognition remain poorly understood. We performed a cohort study of all Swedish men born in 1950 through 1976 who were enlisted for military service at age 18 (N = 1,221,727). Of these, 268,496 were full-sibling pairs, 3,147 twin pairs, and 1,432 monozygotic twin pairs. Physical fitness and intelligence performance data were collected during conscription examinations and linked with other national databases for information on school achievement, socioeconomic status, and sibship. Relationships between cardiovascular fitness and intelligence at age 18 were evaluated by linear models in the total cohort and in subgroups of full-sibling pairs and twin pairs. Cardiovascular fitness, as measured by ergometer cycling, positively associated with intelligence after adjusting for relevant confounders (regression coefficient b = 0.172; 95% CI, 0.168-0.176). Similar results were obtained within monozygotic twin pairs. In contrast, muscle strength was not associated with cognitive performance. Cross-twin cross-trait analyses showed that the associations were primarily explained by individual specific, non-shared environmental influences (>/=80%), whereas heritability explained <15% of covariation. Cardiovascular fitness changes between age 15 and 18 y predicted cognitive performance at 18 y. Cox proportional-hazards models showed that cardiovascular fitness at age 18 y predicted educational achievements later in life. These data substantiate that physical exercise could be an important instrument for public health initiatives to optimize educational achievements, cognitive performance, as well as disease prevention at the society level.
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| 6. |
- Hassing, Linda, 1967, et al.
(författare)
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Overweight in midlife and risk of dementia: a 40-year follow-up study
- 2009
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Ingår i: International Journal of Obesity. - : Springer. ; 33:8, s. 893-898
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Tidskriftsartikel (refereegranskat)abstract
- Objective: This study examines whether overweight in midlife increases dementia risk later in life. Methods: In 1963 body mass index was assessed in 1152 participants of The Swedish Twin Registry, at the age of 45–65 years. These participants were later screened for dementia in a prospective study with up to 40 years follow-up. A total of 312 participants were diagnosed with dementia. Results: Logistic regression analyses adjusted for demographic factors, smoking and alcohol habits, indicated that men and women categorized as overweight in their midlife had an elevated risk of dementia (OR=1.59; 95% CI: 1.21–2.07, P=0.002), Alzheimer's disease (OR=1.71; 95% CI: 1.24–2.35, P=0.003), and vascular dementia (OR=1.55; 95% CI: 0.98–2.47, P=0.059). Further adjustments for diabetes and vascular diseases did not substantially affect the associations, except for vascular dementia (OR=1.36; 95% CI: 0.82–2.56, P=0.116), reflecting the significance of diabetes and vascular diseases in the etiology of vascular dementia. There was no significant interaction between overweight and APOE alt epsilon4 status, indicating that having both risk factors does not have a multiplicative effect with regard to dementia risk. Conclusions: This study gives further support to the notion that overweight in midlife increases later risk of dementia. The risk is increased for both Alzheimer's disease and vascular dementia, and follows the same pattern for men and women. Keywords: BMI, alzheimer's disease, vascular dementia, dementia, overweight, obesity
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| 7. |
- Reynolds, Chandra A, et al.
(författare)
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A survey of ABCA1 sequence variation confirms association with dementia.
- 2009
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Ingår i: Human mutation. - : Hindawi Limited. - 1098-1004 .- 1059-7794. ; 30:9, s. 1348-54
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Tidskriftsartikel (refereegranskat)abstract
- We and others have conducted targeted genetic association analyses of ABCA1 in relation to Alzheimer disease risk with a resultant mixture of both support and refutation, but all previous studies have been based upon only a few markers. Here, a detailed survey of genetic variation in the ABCA1 region has been performed in a total of 1,567 Swedish dementia cases (including 1,275 with Alzheimer disease) and 2,203 controls, providing evidence of association with maximum significance at marker rs2230805 (odds ratio [OR]=1.39; 95% confidence interval [CI] 1.23-1.57, p=7.7x10(-8)). Haplotype-based tests confirmed association of this genomic region after excluding rs2230805, and imputation did not reveal additional markers with greater support. Significantly associating markers reside in two distinct linkage disequilibrium blocks with maxima near the promoter and in the terminal exon of a truncated ABCA1 splice form. The putative risk allele of rs2230805 was also found to be associated with reduced cerebrospinal fluid levels of beta-amyloid. The strongest evidence of association was obtained when all forms of dementia were considered together, but effect sizes were similar when only confirmed Alzheimer disease cases were assessed. Results further implicate ABCA1 in dementia, reinforcing the putative involvement of lipid transport in neurodegenerative disease.
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| 8. |
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| 9. |
- Byrnes, Andrea, et al.
(författare)
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Gene expression in peripheral blood leukocytes in monozygotic twins discordant for chronic fatigue : no evidence of a biomarker
- 2009
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Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 4:6, s. e5805-
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Chronic fatiguing illness remains a poorly understood syndrome of unknown pathogenesis. We attempted to identify biomarkers for chronic fatiguing illness using microarrays to query the transcriptome in peripheral blood leukocytes. METHODS: Cases were 44 individuals who were clinically evaluated and found to meet standard international criteria for chronic fatigue syndrome or idiopathic chronic fatigue, and controls were their monozygotic co-twins who were clinically evaluated and never had even one month of impairing fatigue. Biological sampling conditions were standardized and RNA stabilizing media were used. These methodological features provide rigorous control for bias resulting from case-control mismatched ancestry and experimental error. Individual gene expression profiles were assessed using Affymetrix Human Genome U133 Plus 2.0 arrays. FINDINGS: There were no significant differences in gene expression for any transcript. CONCLUSIONS: Contrary to our expectations, we were unable to identify a biomarker for chronic fatiguing illness in the transcriptome of peripheral blood leukocytes suggesting that positive findings in prior studies may have resulted from experimental bias.
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| 10. |
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