Affiliation: Uppsala University
- Clinical and neuropathological features of the arctic APP gene mutation causing early-onset Alzheimer diseaseHans Basun
Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden
Arch Neurol 65:499-505. 2008..Most of these mutations may also cause cognitive impairment, but the Arctic APP mutation is the only known intra-beta-amyloid mutation to date causing the more typical clinical picture of Alzheimer disease...
- Effects on transthyretin in plasma and cerebrospinal fluid by DHA-rich n - 3 fatty acid supplementation in patients with Alzheimer's disease: the OmegAD studyGerd Faxén-Irving
Department of NVS, Section of Clinical Nutrition, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden
J Alzheimers Dis 36:1-6. 2013..172, p = 0.028). Thus, n - 3 FA treatment appeared to increase plasma-TTR in patients with AD. Since TTR may influence Aβ deposition in the brain, the results warrant further exploration...
- Reduced prostaglandin F2 alpha release from blood mononuclear leukocytes after oral supplementation of omega3 fatty acids: the OmegAD studyInger Vedin
Department of Medicine, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden
J Lipid Res 51:1179-85. 2010..The stimulus-specific PGF(2alpha) release from PBMC after 6 months of oral supplementation with the DHA-rich fish oil might be one event related to reduced inflammatory reactions associated with omega-3 fatty acid intake...
- Omega-3 fatty acids enhance phagocytosis of Alzheimer's disease-related amyloid-β42 by human microglia and decrease inflammatory markersErik Hjorth
Division of Neurodegeneration, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
J Alzheimers Dis 35:697-713. 2013..DHA and EPA can be beneficial in AD by enhancing removal of Aβ42, increasing neurotrophin production, decreasing pro-inflammatory cytokine production, and by inducing a shift in phenotype away from pro-inflammatory M1 activation...
- Effects of DHA-rich n-3 fatty acid supplementation on gene expression in blood mononuclear leukocytes: the OmegAD studyInger Vedin
Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden
PLoS ONE 7:e35425. 2012..Hence, our aim was to determine the effects of 6 mo of dietary supplementation with an n-3 FA preparation rich in DHA on global gene expression in peripheral blood mononuclear cells...
- Effects of supplementation with omega-3 fatty acids on oxidative stress and inflammation in patients with Alzheimer's disease: the OmegAD studyYvonne Freund-Levi
Section of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society NVS, Karolinska Institutet and Department of Geriatrics Karolinska University Hospital Stockholm, Sweden
J Alzheimers Dis 42:823-31. 2014..Omega-3 fatty acids (ω-3 FAs) found in fish and fish oil have several biological properties that may be beneficial in AD. However, they may also auto-oxidize and induce in vivo lipid peroxidation...
- Clinical findings in nondemented mutation carriers predisposed to Alzheimer's disease: a model of mild cognitive impairmentOve Almkvist
Division of Clinical Geriatrics and Experimental Geriatrics, Department of Neurotec, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden
Acta Neurol Scand Suppl 179:77-82. 2003..In conclusion, clinical examinations of relatively young individuals carrying an AD mutation did not reveal any marked abnormalities before the clinical onset of dementia...
- Extended investigation of tau and mutation screening of other candidate genes on chromosome 17q21 in a Swedish FTDP-17 familySusanne Froelich Fabre
Department of Neurotec, Section of Experimental Geriatrics, Karolinska Institutet, Huddinge, Sweden
Am J Med Genet B Neuropsychiatr Genet 121:112-8. 2003..Further investigation of extended intron sequences or promoter regions of the tau gene and additional candidate genes on chromosome 17q21, therefore seems to be necessary in order to identify the additional causes of FTDP-17...
- Nutritional and cognitive relationships and long-term mortality in patients with various dementia disordersGerd Faxén-Irving
Karolinska Institutet, Department of Geriatric Medicine, Karolinska University Hospital, Huddinge, Stockholm, Sweden
Age Ageing 34:136-41. 2005..Subjects with dementia are at risk for protein-energy malnutrition...
- Frontotemporal dementia in a large Swedish family is caused by a progranulin null mutationLena Skoglund
Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden
Neurogenetics 10:27-34. 2009..In conclusion, the PGRN Gly35fs mutation causes frontotemporal dementia with variable clinical presentation in a large Swedish family, most likely through nonsense-mediated decay of mutant PGRN mRNA and resulting haploinsufficiency...
- [Don't underestimate the value of transgenic animal models of Alzheimer disease]Lars N G Nilsson
Lakartidningen 104:798-9; discussion 799-800. 2007
- Cystatin C levels are positively correlated with both Abeta42 and tau levels in cerebrospinal fluid in persons with Alzheimer's disease, mild cognitive impairment, and healthy controlsJohan Sundelöf
Uppsala University, Department of Public Health Geriatrics, Uppsala, Sweden
J Alzheimers Dis 21:471-8. 2010..Interestingly, cystatin C levels were positively correlated with both tau and Abeta42 levels in CSF independent of age, gender, and APOE genotype...
- Higher cathepsin B levels in plasma in Alzheimer's disease compared to healthy controlsJohan Sundelöf
Uppsala University, Department of Public Health Geriatrics, Uppsala, Sweden
J Alzheimers Dis 22:1223-30. 2010..Further investigation of cathepsin B as a predictor of AD is warranted...
- [Conformationally altered proteins cause neurodegenerative diseases]Martin Ingelsson
Geriatriska kliniken, AstraZeneca, Uppsala, Sweden
Lakartidningen 102:3542-3, 3545-6, 3549 passim. 2005..As of today, only symptomatic pharmacotherapies are available, but new insights into the underlying molecular mechanisms are providing strategies to prevent or even cure these devastating disorders...
- Omega-3 fatty acid supplementation effects on weight and appetite in patients with Alzheimer's disease: the omega-3 Alzheimer's disease studyGerd Faxén Irving
Department of Neurobiology, Karolinska Institutet, Karolinska University, Hospital Huddinge, Stockholm, Sweden
J Am Geriatr Soc 57:11-7. 2009..To study the effects of omega (Omega)-3 fatty acid (FA) supplements on weight and appetite in patients with mild to moderate Alzheimer's disease (AD) in relation to inflammatory biomarkers and apolipoprotein E epsilon4 (APOEepsilon4)...
- Plasma levels of Abeta42 and Abeta40 in Alzheimer patients during treatment with the acetylcholinesterase inhibitor tacrineHans Basun
Department of Neurotec, Karolinska Institutet, Huddinge University Hospital, Sweden
Dement Geriatr Cogn Disord 14:156-60. 2002..This finding may indicate that compensatory mechanisms have started at 6 weeks and that no long-term effect on key pathological features in AD is to be expected by an inhibition of acetylcholinesterase...
- Relationship between mercury concentration in blood, cognitive performance, and blood pressure, in an elderly urban populationNina Johansson
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
Biometals 15:189-95. 2002..There was no relation found between B-Hg concentration and cognitive function, arterial BP, age, gender or BMI. In conclusion, no relations were found between B-Hg concentrations and the studied variables...
- Plasma beta amyloid and the risk of Alzheimer disease and dementia in elderly men: a prospective, population-based cohort studyJohan SundelÃ¶f
Uppsala University, Department of Public Health and Geriatrics, Uppsala Science Park, Dag HammarskÃ¶lds vÃ¤g 14B, Uppsala, Sweden
Arch Neurol 65:256-63. 2008..Beta amyloid (Abeta) protein accumulates in the brains of individuals with Alzheimer disease (AD) and is detectable in cerebrospinal fluid and plasma...
- Longitudinal stability of CSF biomarkers in Alzheimer's diseaseKaj Blennow
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Molndal, Sweden
Neurosci Lett 419:18-22. 2007....
- No evidence for tau duplications in frontal temporal dementia families showing genetic linkage to the tau locus in which tau mutations have not been foundJanel Johnson
Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Building 10, Room 6C103, MSC1589, Bethesda, MD 20892, USA
Neurosci Lett 363:99-101. 2004..We did not find any such mutations...
- Effects of docosahexaenoic acid-rich n-3 fatty acid supplementation on cytokine release from blood mononuclear leukocytes: the OmegAD studyInger Vedin
Department of Medicine and the Division of Clinical Nutrition and Metabolism Research, Uppsala University Hospital, Uppsala, Sweden
Am J Clin Nutr 87:1616-22. 2008..Whereas most studies have explored the effects of predominantly EPA-based n-3 FAs preparations, few have addressed the effects of n-3 FAs preparations with DHA as the main FA...
- White matter lesions and soluble interleukin-1 receptor type II in CSF from demented and non-demented subjectsLena Bronge
Department of Radiology, Huddinge University Hospital, S 141 86 Huddinge, Sweden
Neurochem Int 41:217-22. 2002..In conclusion, sIL-1RII levels in CSF are not correlated to magnetic resonance imaging WMLs in patients with dementia disorders or in healthy subjects...
- Determination of isoprostanes in urine samples from Alzheimer patients using porous graphitic carbon liquid chromatography-tandem mass spectrometryKristina Claeson Bohnstedt
Department of Analytical Chemistry, Stockholm University, SE 106 91 Stockholm, Sweden
J Chromatogr B Analyt Technol Biomed Life Sci 796:11-9. 2003..The results from this study support earlier findings that levels of peripheral isoprostanes are not increased in patients with Alzheimer's disease...
- Clinical and molecular aspects of frontotemporal dementiaSusanne Froelich-Fabre
Department of Public Health and Caring Science, Division of Geriatrics, Uppsala University, Uppsala, Sweden
Neurodegener Dis 1:218-24. 2004..However, tau mutations seem to be a rare cause of disease in the general FTD population. Thus, other genes and/or environmental factors are yet to be identified, which will give further clues to this complex and heterogeneous disorder...
- Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trialYvonne Freund-Levi
Department of Neurobiology, Caring Sciences and Society, Section of Clinical Geriatrics, Karolinska University Hospital Huddinge, Stockholm
Arch Neurol 63:1402-8. 2006..Epidemiologic and animal studies have suggested that dietary fish or fish oil rich in omega-3 fatty acids, for example, docosahexaenoic acid and eicosapentaenoic acid, may prevent Alzheimer disease (AD)...
- Omega-3 supplementation in mild to moderate Alzheimer's disease: effects on neuropsychiatric symptomsYvonne Freund-Levi
Department of NVS, Section of Clinical Geriatrics, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden
Int J Geriatr Psychiatry 23:161-9. 2008..An association with APOEomega4 carriers and neuropsychiatric symptoms in AD has also been suggested...