| 1. |
- Brändström, Sven, 1952-, et al.
(author)
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Swedish normative data on personality using the Temperament and Character Inventory
- 1998
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In: Comprehensive Psychiatry. - 0010-440X .- 1532-8384. ; 39:3, s. 122-128
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Journal article (peer-reviewed)abstract
- The Temperament and Character Inventory (TCI) is a self-report personality questionnaire based on Cloninger's psychobiological model of personality, which accounts for both normal and abnormal variation in the two major components of personality, temperament and character. Normative data for the Swedish TCI based on a representative Swedish sample of 1,300 adults are presented, and the psychometric properties of the questionnaire are discussed. The structure of the Swedish version replicates the American version well for the means, distribution of scores, and relationships within the between scales and subscales. Further, the Swedish inventory had a reliable factor structure and test-retest performance. The results of this study confirm the theory of temperament and character as a seven-factor model of personality.
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| 2. |
- Johnstone, Mandy, et al.
(author)
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Copy number variations in DISC1 and DISC1-interacting partners in major mental illness
- 2015
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In: Molecular neuropsychiatry. - : S. Karger AG. - 2296-9209. ; 1:3, s. 175-190
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Journal article (peer-reviewed)abstract
- Robust statistical, genetic and functional evidence supports a role for DISC1 in the aetiology of major mental illness. Furthermore, many of its protein-binding partners show evidence for involvement in the pathophysiology of a range of neurodevelopmental and psychiatric disorders. Copy number variants (CNVs) are suspected to play an important causal role in these disorders. In this study, CNV analysis of DISC1 and its binding partners PAFAH1B1, NDE1, NDEL1, FEZ1, MAP1A, CIT and PDE4B in Scottish and Northern Swedish population-based samples was carried out using multiplex amplicon quantification. Here, we report the finding of rare CNVs in DISC1, NDE1 (together with adjacent genes within the 16p13.11 duplication), NDEL1 (including the overlapping MYH10 gene) and CIT. Our findings provide further evidence for involvement of DISC1 and its interaction partners in neuropsychiatric disorders and also for a role of structural variants in the aetiology of these devastating diseases.
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| 3. |
- Lövdén, Martin, et al.
(author)
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Studying Individual Aging in an Interindividual Context : Typical Paths of Age-Related, Dementia-Related, and Mortality-Related Cognitive Development in Old Age
- 2005
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In: Psychology and Aging. - Washington : American Psychological Association (APA). - 0882-7974 .- 1939-1498. ; 20:2, s. 303-316
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Journal article (peer-reviewed)abstract
- This study has 2 objectives: (a) to explore typical paths of cognitive development associated with aging, terminal decline, and dementia and (b) to promote and illustrate an individual-oriented approach to the study of cognitive aging based on longitudinal panel data from a population-based sample (N = 500; age range-sub(T1)= 60-80, where T refers to time) tested at 3 occasions 5 years apart. Results document interindividual differences in multivariate patterns of change. Although cognitive changes generally covary, the present study indicates that subgroups of individuals develop along different paths characterized by selective changes in subsets of cognitive functions. Typical progression of dementia followed a developmental cascade from low declarative memory, via low functioning across all observed cognitive measures, to dementia diagnosis, and finally, death.
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| 4. |
- Persson, J, et al.
(author)
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Altered brain white-matter integrity in non-demented carriers of the APOE ε4 allele: A risk for Alzheimer’s disease.
- 2006
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In: Neurology. - : Ovid Technologies (Wolters Kluwer Health). - 0028-3878 .- 1526-632X. ; 66:7, s. 1029-1033
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Journal article (peer-reviewed)abstract
- Previous research has shown that polymorphisms of the apolipoprotein E (APOE) represent genetic risk factors for dementia and for cognitive impairment in the elderly. The neural mechanisms by which these genetic variations influence behavioral performance or clinical severity are not well understood. We used diffusion tensor imaging to investigate ultrastructural properties in brain white-matter to detect pathological processes that modify tissue integrity. Sixty participants were included in the study of which 30 were homozygous for the APOE ε3 allele, 10 were homozygous for the APOE ε4 allele, and 20 had the APOE ε34 allele combination. All individuals were non-demented, and the groups were matched on demographic variables and cognitive performance. The results showed a decline in fractional anisotropy, a marker for white-matter integrity, in the posterior corpus callosum of ε4 carriers compared to non-carriers. Additional sites of altered white-matter integrity included the medial temporal lobe. Conclusions: Although the mechanism underlying vulnerability of white matter tracts in APOE ε4 carriers is still unknown, our findings suggest that increased genetic risk for developing AD is associated with changes in microscopic white-matter integrity well before the onset of dementia.
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| 5. |
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| 6. |
- Rademakers, R, et al.
(author)
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Association of cyclin-dependent kinase 5 and neuronal activators p35 and p39 complex in early-onset Alzheimer's disease.
- 2005
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In: Neurobiology of Aging. - New York : Elsevier BV. - 0197-4580 .- 1558-1497. ; 26:8, s. 1145-1151
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Journal article (peer-reviewed)abstract
- Malfunctioning of cyclin-dependent kinase 5 (CDK5) through aberrant proteolytic cleavage of its neuronal activators p35 and p39 is involved in neurodegeneration in Alzheimer's disease (AD) and other neurodegenerative brain diseases. By extensive genetic analysis of the genes encoding CDK5 (CDK5), p35 (CDK5R1) and p39 (CDK5R2), we excluded causal mutations in 70 familial early-onset AD patients. We performed an association study with five informative SNPs in CDK5 in two independent samples of early-onset AD patients and matched control individuals from The Netherlands and northern Sweden. Association was observed with g.149800G>C in intron 5 of CDK5, and a two times increased risk was observed in both patient samples for carriers of the C-allele. Our data are indicative for a role of the CDK5 molecular complex in the genetic etiology of early-onset AD, and suggest that a yet unknown functional variant in CDK5 or in a nearby gene might lead to increased susceptibility for early-onset AD.
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