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  • 1.
    Janelidze, Shorena
    et al.
    Lund University, Lund, Sweden.
    Hertze, Joakim
    Lund University, Lund, Sweden; Skåne University Hospital, Malmö, Sweden.
    Nägga, Katarina
    Lund University, Lund, Sweden; Skåne University Hospital, Malmö, Sweden.
    Nilsson, Karin
    Skåne University Hospital, Malmö, Sweden.
    Nilsson, Christer
    Lund University, Lund, Sweden; Skåne University Hospital, Lund, Sweden.
    Wennström, Malin
    Lund University, Wallenberg Laboratory, Malmö, Sweden.
    van Westen, Danielle
    Lund University, Lund, Sweden; Skåne University Health Care, Lund, Sweden.
    Blennow, Kaj
    the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Sahlgrenska University Hospital, Mölndal, Sweden.
    Zetterberg, Henrik
    the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Sahlgrenska University Hospital, Mölndal, Sweden; UCL Institute of Neurology, Queen Square, London, UK.
    Hansson, Oskar
    Lund University, Lund, Sweden; Skåne University Hospital, Malmö, Sweden.
    Increased blood-brain barrier permeability is associated with dementia and diabetes but not amyloid pathology or APOE genotype2017In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 51, p. 104-112, article id S0197-4580(16)30304-9Article in journal (Refereed)
    Abstract [en]

    Blood-brain barrier (BBB) dysfunction might be an important component of many neurodegenerative disorders. In this study, we investigated its role in dementia using large clinical cohorts. The cerebrospinal fluid (CSF)/plasma albumin ratio (Qalb), an indicator of BBB (and blood-CSF barrier) permeability, was measured in a total of 1015 individuals. The ratio was increased in patients with Alzheimer's disease, dementia with Lewy bodies or Parkinson's disease dementia, subcortical vascular dementia, and frontotemporal dementia compared with controls. However, this measure was not changed during preclinical or prodromal Alzheimer's disease and was not associated with amyloid positron emission tomography or APOE genotype. The Qalb was increased in diabetes mellitus and correlated positively with CSF biomarkers of angiogenesis and endothelial dysfunction (vascular endothelial growth factor, intracellular adhesion molecule 1, and vascular cell adhesion molecule 1). In healthy elderly, high body mass index and waist-hip ratio predicted increased Qalb 20 years later. In summary, BBB permeability is increased in major dementia disorders but does not relate to amyloid pathology or APOE genotype. Instead, BBB impairment may be associated with diabetes and brain microvascular damage.

  • 2.
    Mahler, Jasmin
    et al.
    University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany; University of Tubingen, Germany.
    Morales-Corraliza, Jose
    Nathan S Kline Institute Psychiat Research, NY 10962 USA; NYU, NY USA.
    Stolz, Julia
    University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany; University of Tubingen, Germany.
    Skodras, Angelos
    University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany.
    Radde, Rebecca
    University of Tubingen, Germany.
    Duma, Carmen C.
    University of Tubingen, Germany.
    Eisele, Yvonne S.
    University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany.
    Mazzella, Matthew J.
    Nathan S Kline Institute Psychiat Research, NY 10962 USA.
    Wong, Harrison
    Nathan S Kline Institute Psychiat Research, NY 10962 USA.
    Klunk, William E.
    NYU, NY USA; University of Pittsburgh, PA USA; University of Pittsburgh, PA 15261 USA.
    Nilsson, Peter
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering.
    Staufenbiel, Matthias
    University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany.
    Mathews, Paul M.
    Nathan S Kline Institute Psychiat Research, NY 10962 USA; NYU, NY USA.
    Jucker, Mathias
    University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany.
    Wegenast-Braun, Bettina M.
    University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany.
    Endogenous murine A beta increases amyloid deposition in APP23 but not in APPPS1 transgenic mice2015In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 36, no 7, p. 2241-2247Article in journal (Refereed)
    Abstract [en]

    Endogenous murine amyloid-beta peptide (A beta) is expressed in most A beta precursor protein (APP) transgenic mouse models of Alzheimers disease but its contribution to beta-amyloidosis remains unclear. We demonstrate similar to 35% increased cerebral A beta load in APP23 transgenic mice compared with age-matched APP23 mice on an App-null background. No such difference was found for the much faster A beta-depositing APPPS1 transgenic mouse model between animals with or without the murine App gene. Nevertheless, both APP23 and APPPS1 mice codeposited murine A beta, and immunoelectron microscopy revealed a tight association of murine A beta with human A beta fibrils. Deposition of murine A beta was considerably less efficient compared with the deposition of human A beta indicating a lower amyloidogenic potential of murine A beta in vivo. The amyloid dyes Pittsburgh Compound-B and pentamer formyl thiophene acetic acid did not differentiate between amyloid deposits consisting of human A beta and deposits of mixed human-murine A beta. Our data demonstrate a differential effect of murine A beta on human A beta deposition in different APP transgenic mice. The mechanistically complex interaction of human and mouse A beta may affect pathogenesis of the models and should be considered when models are used for translational preclinical studies.

  • 3.
    Nägga, Katarina
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Geriatric . Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Geriatric Medicine.
    Marcusson, Jan
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Geriatric . Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Geriatric Medicine.
    Effects of cobalamin supplementation - A study on dementia patients with cobalamin deficiency2002In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 23, no 1, p. 427-Conference paper (Other academic)
  • 4.
    Pihlstrøm, Lasse
    et al.
    Oslo University Hospital, Norway .
    Axelsson, Gunnar
    Umeå University, Sweden .
    Bjørnarå, Kari Anne
    Drammen Hospital, Norway .
    Dizdar (Dizdar Segrell), Nil
    Region Östergötland, Center for Diagnostics, Department of Clinical Chemistry.
    Fardell, Camilla
    University of Gothenburg, Sweden .
    Forsgren, Lars
    Umeå University, Sweden .
    Holmberg, Björn
    University of Gothenburg, Sweden .
    Larsen, Jan Petter
    Stavanger University Hospital, Norway .
    Linder, Jan
    Umeå University, Sweden .
    Nissbrandt, Hans
    University of Gothenburg, Sweden .
    Tysnes, Ole-Bjørn
    Haukeland University Hospital, Bergen, Norway.
    Öhman, Eilert
    Umeå University, Sweden .
    Dietrichs, Espen
    Oslo University Hospital, Norway .
    Toft, Mathias
    Oslo University Hospital, Norway .
    Supportive evidence for 11 loci from genome-wide association studies in Parkinson's disease2013In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 34, no 6, p. 1708.e7-1708.e13Article in journal (Refereed)
    Abstract [en]

    Genome-wide association studies have identified a number of susceptibility loci in sporadic Parkinsons disease (PD). Recent larger studies and meta-analyses have greatly expanded the list of proposed association signals. We performed a case-control replication study in a Scandinavian population, analyzing samples from 1345 unrelated PD patients and 1225 control subjects collected by collaborating centers in Norway and Sweden. Single-nucleotide polymorphisms representing 18 loci previously reported at genome-wide significance levels were genotyped, as well as 4 near-significant, suggestive, loci. We replicated 11 association signals at p andlt; 0.05 (SNCA, STK39, MAPT, GPNMB, CCDC62/HIP1R, SYT11, GAK, STX1B, MCCC1/LAMP3, ACMSD, and FGF20). The more recently nominated susceptibility loci were well represented among our positive findings, including 3 which have not previously been validated in independent studies. Conversely, some of the more well-established loci failed to replicate. While future meta-analyses should corroborate disease associations further on the level of common markers, efforts to pinpoint functional variants and understand the biological implications of each risk locus in PD are also warranted.

  • 5.
    Ran, Caroline
    et al.
    Karolinska Institute, Sweden.
    Brodin, Lovisa
    Karolinska University Hospital, Sweden.
    Forsgren, Lars
    Umeå University, Sweden.
    Westerlund, Marie
    Karolinska Institute, Sweden.
    Ramezani, Mehrafarin
    Karolinska Institute, Sweden.
    Gellhaar, Sandra
    Karolinska Institute, Sweden.
    Xiang, Fengqing
    Karolinska University Hospital, Sweden.
    Fardell, Camilla
    University of Gothenburg, Sweden.
    Nissbrandt, Hans
    University of Gothenburg, Sweden.
    Söderkvist, Peter
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
    Puschmann, Andreas
    Skåne University Hospital, Sweden; Lund University, Sweden.
    Ygland, Emil
    Lund University, Sweden.
    Olson, Lars
    Karolinska Institute, Sweden.
    Willows, Thomas
    Karolinska University Hospital, Sweden.
    Johansson, Anders
    Karolinska University Hospital, Sweden.
    Sydow, Olof
    Karolinska University Hospital, Sweden.
    Wirdefeldt, Karin
    Karolinska University Hospital, Sweden; Karolinska Institute, Sweden.
    Galter, Dagmar
    Karolinska Institute, Sweden.
    Svenningsson, Per
    Karolinska University Hospital, Sweden.
    Carmine Belin, Andrea
    Karolinska Institute, Sweden.
    Strong association between glucocerebrosidase mutations and Parkinsons disease in Sweden2016In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 45, no 212.e5Article in journal (Refereed)
    Abstract [en]

    Several genetic studies have demonstrated an association between mutations in glucocerebrosidase (GBA), originally implicated in Gauchers disease, and an increased risk of Parkinsons disease (PD). We have investigated the possible involvement of genetic GBA variations in PD in the Swedish population. Three GBA variants, E326K, N370S, and L444P were screened in the largest Swedish Parkinson cohort reported to date; 1625 cases and 2025 control individuals. We found a significant association with high effect size of the rare variant L444P with PD (odds ratio 8.17; 95% confidence interval: 2.51-26.23; p-value = 0.0020) and a significant association of the common variant E326K (odds ratio 1.60; 95% confidence interval: 1.16-2.22; p-value = 0.026). The rare variant N370S showed a trend for association. Most L444P carriers (68%) were found to reside in northern Sweden, which is consistent with a higher prevalence of Gauchers disease in this part of the country. Our findings support the role of GBA mutations as risk factors for PD and point to lysosomal dysfunction as a mechanism contributing to PD etiology. (C) 2016 The Author(s). Published by Elsevier Inc.

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  • 6.
    Sackmann, Valerie
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Clinical pathology.
    Ansell - Schultz, Anna
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Clinical pathology.
    Sackmann, Christopher
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Clinical pathology.
    Lund, Harald
    Karolinska Hospital Solna, Sweden.
    Harris, Robert A.
    Karolinska Hospital Solna, Sweden.
    Hallbeck, Martin
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Clinical pathology.
    Nilsberth, Camilla
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Local Health Care Services in Central Östergötland, Department of Acute Internal Medicine and Geriatrics.
    Anti-inflammatory (M2) macrophage media reduce transmission of oligomeric amyloid beta in differentiated SH-SY5Y cells2017In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 60, p. 173-182Article in journal (Refereed)
    Abstract [en]

    Neuroinflammation plays an influential role in Alzheimers disease (AD), although the mechanisms underlying this phenomenon remain largely unknown. Microglia are thought to be responsible for the majority of these effects and can be characterized into resting (M0), proinflammatory (M1), or anti-inflammatory (M2) functional phenotypes. We investigated the effects of conditioned macrophage media, as an analogue to microglia, on the transfer of oligomeric amyloid beta (oA beta) between differentiated SH-SY5Y cells. We also investigated how the different inflammatory environments related to intercellular and intracellular changes. We demonstrate that M2 products decrease interneuronal transfer of oA beta, while recombinant interleukin (IL)-4, IL-10, and IL-13 increase transfer. There were no alterations to the mRNA of a number of AD-related genes in response to the combination of oA beta and M0, M1, or M2, but several intracellular proteins, some relating to protein trafficking and the endosomal/lysosomal system, were altered. Stimulating microglia to an M2 phenotype may thus slow down the progression of AD and could be a target for future therapies. (C) 2017 Elsevier Inc. All rights reserved.

  • 7.
    Wikgren, Mikael
    et al.
    Umeå University.
    Karlsson, Thomas
    Linköping University, Department of Behavioural Sciences and Learning. Linköping University, Faculty of Arts and Sciences.
    Nilbrink, Therese
    Umeå University.
    Nordfjall, Katarina
    Umeå University.
    Hultdin, Johan
    Umeå University.
    Sleegers, Kristel
    VIB.
    Van Broeckhoven, Christine
    VIB.
    Nyberg, Lars
    Umeå University.
    Roos, Goran
    Umeå University.
    Nilsson, Lars-Goran
    Stockholm University.
    Adolfsson, Rolf
    Umeå University.
    Norrback, Karl-Fredrik
    Umeå University.
    APOE epsilon 4 is associated with longer telomeres, and longer telomeres among epsilon 4 carriers predicts worse episodic memory2012In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 33, no 2, p. 335-344Article in journal (Refereed)
    Abstract [en]

    Both leukocyte telomere length and the apolipoprotein epsilon 4 allele have been associated with mortality, cardiovascular disease, cognition, and dementia. The authors investigated whether leukocyte telomere length was associated with APOE genotype or cognitive abilities in the context of APOE genotype. The setting for this cross-sectional study was 427 nondemented individuals aged 41-81 yr. The authors found that epsilon 4 carriers overall exhibited significantly longer telomeres compared with non-carriers (difference of 268 bp, p = 0.001). This difference was greatest at the lower limit of the age span and nonsignificant at the upper limit, which translated into a significantly higher telomere attrition rate (p = 0.049) among epsilon 4 carriers (37 bp/years) compared with non-carriers (21 bp/year). Further, longer telomeres among epsilon 4 carriers significantly predicted worse performance on episodic memory tasks. No significant associations were found on tasks tapping semantic and visuospatial ability, or among epsilon 3/epsilon 3 carriers. In conclusion, APOE epsilon 4 carriers had longer telomeres compared with non-carriers, but higher rate of attrition. Among them, longer telomeres predicted worse performance on episodic memory tasks. These observations suggest that the epsilon 4 allele is associated with abnormal cell turnover of functional and possibly clinical significance.

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