| 1. |
- Olsson, Lars-Eric, 1951, et al.
(author)
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Höftfraktur
- 2009
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In: Prehospital akutsjukvård Redaktörer Leif Svensson Björn-Ove Suserud. - Stockholm : Liber. - 9789147084487 ; , s. 428-434
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Book chapter (other academic/artistic)
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| 2. |
- Lindén, Thomas, 1962
(author)
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Demens efter stroke.
- 2007
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In: E-publikation Vårdalinstitutets hemsida "Tematiska rum" 2007.
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Journal article (other academic/artistic)
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| 3. |
- Lindén, Thomas, 1962, et al.
(author)
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Plasticitet, kognition och rehabilitering
- 2009
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In: Peter-Eriksson-symposiet "Den Stressade Hjärnan", Göteborg, december 2009.
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Conference paper (other academic/artistic)
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| 4. |
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| 5. |
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| 6. |
- Johansson, Annica, 1969, et al.
(author)
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CYP46A1 Variants Interact with Age and APOE to Influence CSF Aβ42 and Phospho-Tau Levels in Alzheimer's Disease
- 2004
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In: The 9th International Conference on Alzheimer's Disease (ICAD), Philadelphia, Pennsylvania, USA, 20-25 July 2004.
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Conference paper (other academic/artistic)abstract
- Recent studies have suggested that variants of CYP46A1, encoding cholesterol 24-hydroxylase (CYP46), confer risk to Alzheimer's disease (AD), a prospect substantiated by evidence of genetic association with several quantitative traits related to AD pathology, including cerebrospinal fluid (CSF) levels of the 42 amino-acid cleavage product of β-amyloid (Aβ42) and the tau protein. In the present study, these claims have been explored by the genotyping of previously associated markers in CYP46A1 in three independent Northern European case-control series encompassing 1323 individuals, which include approximately 400 patients with measures of CSF Aβ42 and phospho-tau protein levels. Tests of association in case-control models revealed limited evidence that CYP46A1 variants contribute to AD risk across these samples. However, models testing for potential effects upon CSF measures suggested possible interaction of an intronic marker (rs754203) with age and APOE genotype. In stratified analyses, significant effects were evident that were restricted to elderly APOE ε4 carriers for both CSF Aβ42 (P = 0.0009) and phospho-tau (P = 0.046). Computational analyses indicate that the rs754203 marker probably does not impact the binding of regulatory factors, suggesting that other polymorphic sites underlie observed associations. Results provide an important independent replication of previous findings, supporting the existence of CYP46A1 sequence variants that contribute to variability in β-amyloid metabolism.
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| 7. |
- Johansson, Annica, 1969, et al.
(author)
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Homocysteine levels in patients with Alzheimer's disease are influenced by the glutathione s-transferase omega-1 (GSTO1) gene
- 2005
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In: Haematologica Reports. - 1824-9337. ; 2005:1(3):June
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Conference paper (other academic/artistic)abstract
- Background: A substantial body of literature confirms an association between elevated blood levels of homocysteine and cognitive dysfunction, including Alzheimer’s disease (AD). Oxidative stress is a risk factor for AD. Elevated homocysteine levels might partially reflect redox status; its remethylation to methionine is coordinated by the redox-sensitive enzyme methionine synthase. Glutathione S-transferase omega-1 (GSTO1) is protective against oxidative stress, and the polymorphism Ala140Asp modifies the age-of-onset of AD. Aim: To investigate whether the GSTO1 Ala140Asp polymorphism is related to homocysteine levels in AD patients. Methods: Plasma homocysteine levels and the GSTO1 polymorphism Ala140Asp were analysed in 244 consecutive patients with clinically diagnosed AD. Results: Homocysteine levels differed significantly between the three genotypes (p=0.002) analysis of variance, Durbin-Watson D Statistic. The levels were 11.8±3.6 µmol/L in patients with the Ala/Ala genotype (n=118), 13.5±5.0 µmol/L in the Ala/Asp group (n=105), and 14.1±6.0 µmol/L in patients with the Asp/Asp genotype (n=21). Carriers of at least one Asp allele showed significantly higher plasma homocysteine levels compared to non-carriers (p=0.002) two-sample t-test. Conclusion: The association between homocysteine levels and this GSTO1 polymorphism supports the suggestion that increased homocysteine in AD patients may be a consequence of oxidative stress.
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| 8. |
- Johansson, Annica, 1969, et al.
(author)
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Identification of polymorphic sites in the CDC2 gene, a possible susceptibility gene for Alzheimer's disease located on chromosome 10
- 2002
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In: The 8th International Conference on Alzheimer's Disease and Related Disorders, Stockholm 20-25 July 2002.
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Conference paper (other academic/artistic)abstract
- The human cdc2, which is required in the mitotic cell cycle, has recently been associated with Alzheimer’s disease (AD). Cdc2 has also been shown to phosphorylate all of tau protein, β-amyloid and amyloid precursor protein (APP) both in vitro and in vivo. Inappropriate activation of cdc2 kinase in differentiated neurons has been suggested to contribute to neuronal dysfunction and degeneration in AD. The cdc2 gene maps to chromosome 10q, which recently has been found to be a susceptibility locus for AD, which makes the cdc2 gene a possible candidate gene for AD. To investigate whether the cdc2 gene contains polymorphic sites we sequenced the promoter region and the seven coding exons and flanking introns in 14 AD cases and 8 controls. We found several variations in the promoter region and three polymorphic sites in the intron between exon 6 and 7, one of these located in the 5’-splice site of exon 6. Data will be presented on the frequency of these polymorphisms in large series of AD patients and controls.
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| 9. |
- Johansson, Annica, 1969
(author)
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Susceptibility Genes in Alzheimer’s Disease: Associations and Mechanisms
- 2004
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Licentiate thesis (other academic/artistic)abstract
- Alzheimer’s disease (AD) is the most common form of dementia, followed by frontotemporal dementia (FTD), in the elderly. It is a genetically heterogeneous disease characterized by progressive cognitive decline and memory impairment. In the rare early-onset familial form of the disease (FAD), causative mutations have been found in three different genes, the amyloid precursor protein (APP) gene and the presenilins 1 and 2 (PSEN-1 and -2). The predominant late-onset form of AD (LOAD) is a genetically complex disorder probably involving a combination of genetic factors together with environmental influences. To date, the only genetic risk factor identified for this complex form of AD is the APOE-ε4 allele. This only account for a fraction of all AD cases, thus several susceptibility genes remain to be found. The overall aim of this thesis is to study potential candidate genes for AD and FTD, and to see how variants of these genes influence quantitative traits related to AD pathology, both in cerebrospinal fluid (CSF), and in brain tissue. In the initial investigation, a polymorphism designated Ex6+7I/D in the cell division cycle (CDC2) gene was identified. Cdc2 is a protein kinase involved in cell cycle regulation and in neuronal differentiation. In AD brain, cdc2 is expressed in neurons and is involved in the abnormal phosphorylation of tau. The polymorphism was tested for association with LOAD. A significant association between the Ex6+7II genotype and AD was found, and also an increased frequency of the Ex6+7I allele in both AD and FTD. In the second paper, variants of CYP46A1, encoding cholesterol 24-hydroxylase (CYP46), were investigated for their association with AD. The polymorphisms were tested for association with quantitative traits related to AD pathology, including cerebrospinal fluid (CSF) levels of the 42 amino-acid cleavage product of β-amyloid (β-amyloid1-42), and the tau protein. In stratified analyses, one of the polymorphisms (rs754203) significantly influenced both CSF β-amyloid1-42 and phospho-tau in elderly APOE-ε4 carriers. In the final paper, AD and FTD patients were genotyped for a polymorphism in the Saitohin (STH) gene, a previously described gene located in the intron of the human Tau gene. Numerous polymorphisms span the human tau gene and are in complete linkage disequilibrium with each other yielding two separate haplotypes, termed H1 and H2. The H1 haplotype has been associated with both AD and FTD, and our patients were also investigated for this haplotype. In all patients (AD and FTD) and controls, the STH polymorphism and the Tau haplotype were in complete disequilibrium. The Tau haplotype and STH were not associated with AD and FTD, neither did they influence CSF-levels of total-tau, phospho-tau and β-amyloid1-42, nor neuropathological scores of plaque and tangles in brain tissue.
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| 10. |
- Andin, Ulla
(author)
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Vascular dementia - classification and clinical correlates
- 2007
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Doctoral thesis (other academic/artistic)abstract
- During the period (1976-1995) a total of 175 consecutive patients (m 88/f 87) with neuropathologically verified vascular dementia (VaD) were examined. 22 patients with pure Alzheimer's Disease (AD) were also studied. All patients were diagnosed and followed at the Department of Psychogeriatrics (Lund University Hospital). The neuropathological examination revealed VaD, sometimes with additional contribution of Alzheimer pathology. The cases were classified as Large Vessel Dementia (LVD), Small Vessel Dementia (SVD) and Hypoperfusive Hypoxic-ischemic Dementia (HHD). The mean age at death was 80 years (range 54-100) and almost identical in the three groups.The results show that VaD is neuropathologically heterogeneous, characterized by one, two or all three types of vascular pathology. The majority of cases (126/175), showed more than one type of brain pathology (vascular or in combination with Alzheimer pathology). There was a large coexistence with Alzheimer pathology (65% of the total 175 cases). 49 cases were pure, with only one type of vascular pathology. SVD was the largest pure group (21% of the total 175 cases). Post mortem verified heart pathology, was twice as common in SVD as in LVD and HHD.Cardio-cerebrovascular features (arrhythmia, congestive heart failure, cardiac infarction, hypertension, orthostatic hypotension and TIA/stroke) were more common in LVD and SVD, than in HHD. The coexistence of Alzheimer pathology did not change these results.Dizziness and unsteadiness or falls were reported in 102 of the 175 VaD patients. Dizziness correlated with hypertension and orthostatic hypotension while unsteadiness correlated only with hypertension. Falls correlated strongly to the use of neuroleptics and hypnotics.Hallucinations/delusions and delirium were reported in many patients and most common in the groups with pure LVD, pure SVD and especially in the SVD with combined Alzheimer pathology.Cardio-cerebrovascular features were more common in patients with AD combined with white matter pathology than those with pure AD. This study illustrates the neuropathological and clinical heterogeneity in VaD. This is of great importance for the understanding, treatment and care of the individual suffering from VaD.
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