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  • 1.
    Bloniecki, Victor
    et al.
    Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institute, Stockholm, Sweden.
    Aarsland, Dag
    Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institute, Stockholm, Sweden; Department of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden; Center for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway.
    Blennow, Kaj
    Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
    Cummings, Jeffrey
    Cleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, NV, USA.
    Falahati, Farshad
    Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institute, Stockholm, Sweden.
    Winblad, Bengt
    Department of Neurobiology, Caring Sciences and Society (NVS), Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institute, Huddinge, Sweden.
    Freund-Levi, Yvonne
    Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institute, Stockholm, Sweden; Department of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Effects of Risperidone and Galantamine Treatment on Alzheimer's Disease Biomarker Levels in Cerebrospinal Fluid2017In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 57, no 2, p. 387-393Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Treatment for neuropsychiatric symptoms (NPS) in dementia is insufficient. Antipsychotics and acetylcholinesterase inhibitors are used generating symptomatic improvements in behavior and cognition, but few studies have investigated their effect on Alzheimer's disease (AD) biomarkers in cerebrospinal fluid (CSF).

    OBJECTIVE: This is a secondary analysis based on an earlier clinical trial comparing the treatment effects on NPS. The aim of this study was to examine whether treatment with risperidone and galantamine affect levels of the biomarkers T-Tau, P-Tau, Aβ1-42, and Aβ42/40-ratio in CSF. The secondary aim was to test if baseline levels of these biomarkers are associated with the clinical course of NPS.

    METHODS: 83 patients (mean + SD 77.9.6±7.7 years) with dementia and NPS were randomized to galantamine (n = 44) or risperidone (n = 39) treatment. CSF samples were collected at baseline and after 12 weeks.

    RESULTS: Changes in levels of biomarkers between the two treatment groups did not differ significantly. Low baseline levels of Aβ1 - 42 was significantly associated with reduction of irritability at follow up. Low baseline levels of Aβ1-42, Aβ42/40, and P-Tau were significant correlates of reduction in appetite and eating disorders. CSF Aβ1-42 levels in patients treated with risperidone were significantly decreased at follow up, showing an 8% (40 pg/mL) reduction as compared with baseline (p = 0.03).

    CONCLUSIONS: Our results suggest that risperidone may affect the CSF profile of AD biomarkers indicating more amyloid pathology. Treatment with galantamine did not affect the CSF biomarkers in any direction. The AD CSF biomarkers displayed correlations with specific NPS suggesting potential research questions to be pursued.

  • 2.
    Eriksdotter, Maria
    et al.
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Stockholm; Department of Geriatric Medicine, Karolinska University Hospital, Huddinge, Stockholm.
    Vedin, Inger
    Department of Medicine, Division of Hematology, Karolinska Institutet, Huddinge, Stockholm.
    Falahati, Farshad
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Stockholm.
    Freund-Levi, Yvonne
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Stockholm.
    Hjorth, Erik
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Neurodegeneration, Karolinska Institutet, Huddinge, Stockholm.
    Faxen-Irving, Gerd
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Stockholm.
    Wahlund, Lars-Olof
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Stockholm; Department of Geriatric Medicine, Karolinska University Hospital, Huddinge, Stockholm.
    Schultzberg, Marianne
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Neurodegeneration, Karolinska Institutet, Huddinge, Stockholm.
    Basun, Hans
    Division of Geriatrics, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden; Department of Geriatric Medicine, Akademiska sjukhuset, Uppsala, Sweden.
    Cederholm, Tommy
    Division of Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden; Department of Geriatric Medicine, Akademiska sjukhuset, Uppsala, Sweden.
    Palmblad, Jan
    Department of Medicine, Division of Hematology, Karolinska Institutet, Huddinge, Stockholm.
    Plasma Fatty Acid Profiles in Relation to Cognition and Gender in Alzheimer's Disease Patients During Oral Omega-3 Fatty Acid Supplementation: The OmegAD Study2015In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 48, no 3, p. 805-812Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: ω3 fatty acids (ω3 FAs) may slow the rate of decline in cognitive performance in mild forms of cognitive impairment and Alzheimer's disease (AD). However, the relationship between changes of plasma ω3 FA levels and cognitive performance, as well as effects of gender, are poorly known.

    OBJECTIVE: To study the effect of 6-month administration of DHA-rich ω3 FA supplementation on plasma FA profiles in patients with mild to moderate AD in relation to cognitive performance and gender. This investigation is part of the OmegAD Study.

    METHODS: 174 AD patients (74 ± 9 years) were randomized to a daily intake of 2.3 g ω3 FA or placebo for 6 months; subsequently all received the ω3 FA preparation for the next 6 months. Baseline as well as changes in plasma levels of the main ω3 FAs in 165 patients, while receiving ω3 FA supplementation for 6 months, were analyzed for association to cognitive performance (assessed by ADAS-cog and MMSE scores) as well as to gender.

    RESULTS: Preservation of cognitive functioning, assessed by ADAS-cog or its sub-items (but not MMSE) scores, was significantly associated to increasing plasma ω3 FA levels over time. Thus, the higher ω3 FA plasma levels rose, the lower was the rate of cognitive deterioration. This effect was not related to gender; since although females displayed higher ω3 FA plasma levels than did males after 6 months of supplementation, this difference disappeared when adjusted for body weight.

    CONCLUSIONS: Since our study suggests dose-response relationships between plasma levels of ω3 FA and preservation of cognition, future ω3 FA trials in patients with mild AD should consider exploring graded (and body weight adjusted) doses of ω3 FA.

  • 3.
    Faxen-Irving, Gerd
    et al.
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Sweden.
    Falahati, Farshad
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Sweden.
    Basun, Hans
    Department of Public Health and Caring Sciences, Division of Geriatrics, Uppsala University, Uppsala, Sweden.
    Eriksdotter, Maria
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Sweden; Department of Geriatrics, Karolinska University Hospital, Huddinge, Sweden.
    Vedin, Inger
    Department of Medicine, Division of Hematology, Department of NVS, Karolinska Institutet, Huddinge, Sweden.
    Wahlund, Lars-Olof
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Sweden; Department of Geriatrics, Karolinska University Hospital, Huddinge, Sweden.
    Schultzberg, Marianne
    Division of Neurodegeneration, Karolinska Institutet, Huddinge, Sweden.
    Hjorth, Erik
    Division of Neurodegeneration, Karolinska Institutet, Huddinge, Sweden.
    Palmblad, Jan
    Department of Medicine, Division of Hematology, Department of NVS, Karolinska Institutet, Huddinge, Sweden.
    Cederholm, Tommy
    Department of Public Health and Caring Sciences, Division of Clinical Nutrition and Metabolism, Uppsala University, Uppsala, Sweden; Department of Geriatric Medicine, Akademiska sjukhuset, Uppsala, Sweden.
    Freund-Levi, Yvonne
    Department of Neurobiology, Care Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Sweden; Department of Geriatrics, Karolinska University Hospital, Huddinge, Sweden.
    Does Fatty Acid Composition in Subcutaneous Adipose Tissue Differ between Patients with Alzheimer's Disease and Cohabiting Proxies?2018In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 61, no 2, p. 515-519Article in journal (Refereed)
    Abstract [en]

    Low tissue levels of the major marine ω3 fatty acids (FAs) DHA and EPA are found in Alzheimer's disease (AD). We investigated if healthy proxies to AD patients have higher levels of these ω3 FAs. We observed lower levels of EPA and DHA in subcutaneous adipose tissue biopsies from 64 AD patients compared with 16 cognitively healthy proxies. No significant difference was observed when pairwise comparisons were made between a subset of 16 AD patients and their co-habiting proxies. Larger studies are needed to replicate these findings and to determine if they could depend on FA intake or differences in metabolism.

  • 4.
    Faxén-Irving, Gerd
    et al.
    Department of NVS, Section of Clinical Nutrition, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Freund-Levi, Yvonne
    Department of NVS, Section of Clinical Geriatrics, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Eriksdotter-Jönhagen, Maria
    Department of NVS, Section of Clinical Geriatrics, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Basun, Hans
    Department of Public Health and Caring Sciences, Division of Geriatrics, Uppsala University Hospital, Uppsala, Sweden.
    Hjorth, Erik
    Department of NVS, Section of Clinical Nutrition, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Palmblad, Jan
    Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Vedin, Inger
    Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Cederholm, Tommy
    Department of Public Health and Caring Sciences, Division of Clinical Nutrition and Metabolism, Uppsala University Hospital, Uppsala, Sweden.
    Wahlund, Lars-Olof
    Department of NVS, Section of Clinical Geriatrics, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Effects on transthyretin in plasma and cerebrospinal fluid by DHA-rich n - 3 fatty acid supplementation in patients with Alzheimer's disease: the OmegAD study2013In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 36, no 1, p. 1-6Article in journal (Refereed)
    Abstract [en]

    Transthyretin (TTR) binds amyloid-β (Aβ) and may reduce brain Aβ, a pathological feature in Alzheimer's disease (AD). N - 3 fatty acids (FA), docosahexaenoic (DHA), and eicosapentaenoic acid (EPA) may increase TTR transcription in rat hippocampus. We studied effects of n - 3 FA supplementation on TTR-levels in patients with AD. Outpatients were randomized to receive 1.7 g DHA and 0.6 g EPA (n - 3/n - 3 group) or placebo (placebo/n - 3 group) during 6 months. After 6 months, all patients received n - 3 FA for another 6 months. TTR and FA were measured in plasma in all subjects, whereas TTR in cerebrospinal fluid (CSF) was measured in a subgroup. The study was completed by 89 patients in the n - 3/n - 3 group (75 y, 57% w) and 85 in the placebo/n - 3 group (75 y, 46% w). Baseline plasma-TTR was within normal range in both groups. After 6 months, plasma-TTR decreased in the placebo/n - 3 group (p < 0.001 within and p < 0.015 between the groups). No changes were observed in CSF TTR. From 6 to 12 months when both groups were supplemented, plasma-TTR increased significantly in both groups. Repeated measures ANOVA indicated an increase in TTR over time (p = 0.04) in those receiving n - 3 FA for 12 months. By linear regression analyses, n - 3 FA treatment was independently associated with increased plasma-TTR at 6 months (β = -0.172, 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.

  • 5.
    Freund-Levi, Yvonne
    et al.
    Section of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet and Department of Geriatrics Karolinska University Hospital Stockholm, Sweden.
    Vedin, Inger
    Division of Haematology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Hjorth, Erik
    Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Basun, Hans
    Division of Geriatrics, Uppsala University, Uppsala, Sweden; Chaire d'Excellence Program, Department of Biochemistry, Molecular Biology and Nutrition, Universite d'Auvergne, Clermont-Ferrand, France.
    Faxén Irving, Gerd
    Divisions of Clinical Nutrition, Karolinska Institutet, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Schultzberg, Marianne
    Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Eriksdotter, Maria
    Section of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet and Department of Geriatrics Karolinska University Hospital Stockholm, Sweden.
    Palmblad, Jan
    Division of Haematology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Vessby, Bengt
    Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
    Wahlund, Lars-Olof
    Section of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet and Department of Geriatrics Karolinska University Hospital Stockholm, Sweden.
    Cederholm, Tommy
    Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
    Basu, Samar
    Division of Oxidative Stress and Inflammation, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden; Chaire d'Excellence Program, Department of Biochemistry, Molecular Biology and Nutrition, Universite d'Auvergne, Clermont-Ferrand, France.
    Effects of supplementation with omega-3 fatty acids on oxidative stress and inflammation in patients with Alzheimer's disease: the OmegAD study2014In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 42, no 3, p. 823-831Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Oxidative stress and inflammation are two key mechanisms suggested to be involved in the pathogenesis of Alzheimer's disease (AD). 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.

    OBJECTIVE: The objective of this study was to evaluate systemic oxidative stress and inflammatory biomarkers following oral supplementation of dietary ω-3 FA.

    METHODS: Forty patients with moderate AD were randomized to receive 1.7 g DHA (22:6) and 0.6 g EPA (20:5) or placebo for 6 months. Urinary samples were collected before and after supplementation. The levels of the major F2-isoprostane, 8-iso-PGF2α, a consistent in vivo biomarker of oxidative stress, and 15-keto-dihydro-PGF2α, a major metabolite of PGF2α and biomarker of inflammatory response, were measured.

    RESULTS: F2-isoprostane in urine increased in the placebo group after 6 months, but there was no clear difference in treatment effect between supplemented and non-supplemented patients on the urinary levels of F2-isoprostanes and 15-keto-dihydro-PGF2α. At baseline, the levels of 15-keto-dihydro-PGF2α showed negative correlative relationships to ω-3 FAs, and a positive correlation to linoleic acid. 8-iso-PGF2α correlated negatively to the ω-6 FA arachidonic acid.

    CONCLUSION: The findings indicate that supplementation of ω-3 FAs to patients with AD for 6 months does not have a clear effect on free radical-mediated formation of F2-isoprostane or cyclooxygenase-mediated formation of prostaglandin F2α. The correlative relationships to FAs indicate a potential role of FAs in immunoregulation.

  • 6.
    Hjorth, Erik
    et al.
    Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Zhu, Mingqin
    Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Toro, Veronica Cortés
    Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Vedin, Inger
    Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Palmblad, Jan
    Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Cederholm, Tommy
    Division of Clinical Nutrition and Metabolism, Department of Public Health & Caring Sciences, Uppsala University Hospital, Uppsala, Sweden.
    Freund-Levi, Yvonne
    Clinical Geriatrics, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Faxen-Irving, Gerd
    Nutrition, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Wahlund, Lars-Olof
    Clinical Geriatrics, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Basun, Hans
    Division of Geriatrics, Department of Public Health & Caring Sciences, Uppsala University Hospital, Uppsala, Sweden.
    Eriksdotter, Maria
    Clinical Geriatrics, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Schultzberg, Marianne
    Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
    Omega-3 fatty acids enhance phagocytosis of Alzheimer's disease-related amyloid-β42 by human microglia and decrease inflammatory markers2013In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 35, no 4, p. 697-713Article in journal (Refereed)
    Abstract [en]

    The use of supplements with omega-3 (ω3) fatty acids (FAs) such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) is widespread due to proposed beneficial effects on the nervous and cardiovascular systems. Many effects of ω3 FAs are believed to be caused by down-regulation and resolution of inflammation. Alzheimer's disease (AD) is associated with inflammation mediated by microglia and astrocytes, and ω3 FAs have been proposed as potential treatments for AD. The focus of the present study is on the effects of DHA and EPA on microglial phagocytosis of the AD pathogen amyloid-β (Aβ), on secreted and cellular markers of immune activity, and on production of brain-derived neurotrophic factor (BDNF). Human CHME3 microglial cells were exposed to DHA or EPA, with or without the presence of Aβ42. Phagocytosis of Aβ42 was analyzed by flow cytometry in conjunction with immunocytochemistry using antibodies to cellular proteins. Secreted proteins were analyzed by ELISA. Both DHA and EPA were found to stimulate microglial phagocytosis of Aβ42. Phagocytosis of Aβ42 was performed by microglia with a predominance of M2 markers. EPA increased the levels of BDNF in the culture medium. The levels of TNF-α were decreased by DHA. Both DHA and EPA decreased the pro-inflammatory M1 markers CD40 and CD86, and DHA had a stimulatory effect on the anti-inflammatory M2 marker CD206. 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.

  • 7.
    Jernerén, Fredrik
    et al.
    Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden.
    Cederholm, Tommy
    Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden; Theme Ageing, Karolinska University Hospital, Stockholm, Sweden.
    Refsum, Helga
    Department of Nutrition, University of Oslo, Oslo, Norway; Department of Pharmacology, University of Oxford, Oxford, United Kingdom.
    Smith, A. David
    Department of Pharmacology, University of Oxford, Oxford, United Kingdom.
    Turner, Cheryl
    Department of Pharmacology, University of Oxford, Oxford, United Kingdom.
    Palmblad, Jan
    Departments of Medicine and Hematology, Karolinska University Hospital Huddinge, and the Karolinska Institutet, Stockholm, Sweden.
    Eriksdotter, Maria
    Theme Ageing, Karolinska University Hospital, Stockholm, Sweden; Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Hjorth, Erik
    Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Faxen-Irving, Gerd
    Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Wahlund, Lars-Olof
    Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Schultzberg, Marianne
    Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Basun, Hans
    Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
    Freund-Levi, Yvonne
    Örebro University, School of Medical Sciences. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden; Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Sweden; Department of Psychiatry in Region Örebro County and School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro; Department of Old Age Psychiatry, Psychology & Neuroscience, King’s College, London, UK.
    Homocysteine Status Modifies the Treatment Effect of Omega-3 Fatty Acids on Cognition in a Randomized Clinical Trial in Mild to Moderate Alzheimer's Disease: The OmegAD Study2019In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 69, no 1, p. 189-197Article in journal (Refereed)
    Abstract [en]

    Background: Trials of supplementation with omega-3 fatty acids (omega 3-FAs) in patients with mild cognitive impairment or Alzheimer's disease (AD) have produced inconsistent effects on cognitive decline. There is evidence of an interaction between B vitamin status and omega 3-FAs in relation to brain atrophy and cognitive decline.

    Objective: We investigated whether baseline levels of plasma total homocysteine (tHcy), a marker of B vitamin status, modify the effects of omega 3-FAs supplementation on cognitive performance in moderate AD.

    Methods: This post hoc analysis of the OmegAD trial included 171 community-based patients with AD (MMSE >= 15): 88 patients received daily doses of 1.7 g docosahexaenoic acid and 0.6 g eicosapentaenoic acid for 6 months. Treatment outcome on cognition was analyzed according to baseline levels of tHcy using a general linear model and ANCOVA.

    Results: We found significant interactions between omega 3-FA supplementation and tHcy on cognition and clinical stage assessed by MMSE (p = 0.040), global CDR (p = 0.059), and CDRsob (p = 0.023), but not on ADAS-cog (p = 0.649). In patients with tHcy levels <11.7 mu mol/L, omega 3-FA supplementation improved cognitive performance as measured by MMSE (+7.1%, 95% CI: 0.59 to 13.7%, p = 0.033) and clinical status as measured by CDRsob (-22.3%, 95% CI: -5.8 to -38.7%, p = 0.009) compared with placebo.

    Conclusion: The effect of omega 3-FA supplementation on MMSE and CDR appears to be influenced by baseline tHcy, suggesting that adequate B vitamin status is required to obtain beneficial effects of omega 3-FA on cognition.

  • 8.
    Lebwohl, Benjamin
    et al.
    Dept Med, Celiac Dis Ctr, Columbia Univ Coll Phys & Surg, New York NY, USA; Dept Med Epidemiol & Biostat, Karolinska Univ Hosp, Stockholm, Sweden; Karolinska Institute, Stockholm, Sweden; Dept Med, Columbia Univ Coll Phys & Surg, New York, NY, USA; Med Ctr, Mailman Sch Publ Hlth, Dept Epidemiol, Columbia Univ, New York NY, USA.
    Luchsinger, Jose A.
    Dept Med, Columbia Univ Coll Phys & Surg, New York NY, USA; Med Ctr, Mailman Sch Publ Hlth, Dept Epidemiol, Columbia Univ, New York NY, USA.
    Freedberg, Daniel E.
    Dept Med, Columbia Univ Coll Phys & Surg, New York NY, USA.
    Green, Peter H. R.
    Dept Med, Celiac Dis Ctr, Columbia Univ Coll Phys & Surg, New York NY, USA.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Med Epidemiol & Biostat, Karolinska Univ Hosp, Stockholm, Sweden; Karolinska Inst, Stockholm, Sweden; Dept Pediat, Örebro University Hospital, Örebro, Sweden.
    Risk of Dementia in Patients with Celiac Disease: A Population-Based Cohort Study2016In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 49, no 1, p. 179-185Article in journal (Refereed)
    Abstract [en]

    Background: Patients with celiac disease (CD) frequently report cognitive symptoms when they are exposed to gluten, and cognitive deficits have been quantified in patients with newly diagnosed CD. Objective: To determine whether patients with CD have an increased risk of dementia. Methods: Using a population-based database of older adults (age >= 50 years) with histologically proven CD (duodenal/jejunal villous atrophy) from all 28 pathology departments in Sweden, we compared the incidence of a subsequent dementia diagnosis to those of age-and gender-matched controls. Results: Among patients with CD (n = 8,846) and controls (n = 43,474), the median age was 63 years and 56% were female. During a median follow-up time of 8.4 years, dementia was diagnosed in 4.3% of CD patients and 4.4% of controls (HR 1.07; 95% CI 0.95-1.20). Although there was an increased risk of dementia in the first year following a diagnosis of CD (HR 1.73; 95% CI 1.15-2.61), this risk was not present in the whole observation period. Among those subjects with a dementia subtype specified, the increased risk was restricted to vascular dementia (HR 1.28; 95% CI 1.00-1.64) and was not present for Alzheimer's dementia (HR 1.12; 95% CI 0.91-1.37). Conclusions: Patients with CD are not at increased risk for dementia overall, though subgroup analysis suggests that they may be at increased risk for vascular dementia.

  • 9.
    Reijs, Babette L R
    et al.
    Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Vos, Stephanie J B
    Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Soininen, Hilkka
    Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland; Department of Neurology, Kuopio University Hospital, Kuopio, Finland.
    Lötjonen, Jyrki
    VTT Technical Research Centre of Finland, Tampere, Finland; Combinostics Oy, Tampere, Finland.
    Koikkalainen, Juha
    VTT Technical Research Centre of Finland, Tampere, Finland; Combinostics Oy, Tampere, Finland.
    Pikkarainen, Maria
    Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland.
    Hall, Anette
    Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland.
    Vanninen, Ritva
    Department of Radiology, Kuopio University Hospital, Kuopio, Finland.
    Liu, Yawu
    Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland; Department of Radiology, Kuopio University Hospital, Kuopio, Finland.
    Herukka, Sanna-Kaisa
    Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland; Department of Neurology, Kuopio University Hospital, Kuopio, Finland.
    Freund-Levi, Yvonne
    Örebro University, School of Medical Sciences. Department of NVS, Section of Clinical Geriatrics, Karolinska Institutet, Karolinska University Hospital, Huddinge, Sweden.
    Frisoni, Giovanni B
    LENITEM, IRCCS Fatebenefratelli, Brescia.
    Frölich, Lutz
    Department of Geriatric Psychiatry, Medical Faculty Mannheim, University of Heidelberg, Germany.
    Nobili, Flavio
    Department of Neuroscience (DINOGMI), Clinical Neurology, University of Genoa and IRCCS AOU San Martino-IST Genoa, Italy.
    Rikkert, Marcel Olde
    Department of Geriatrics, Radboud University Medical Centre, Nijmegen, The Netherlands.
    Spiru, Luiza
    Carol Davila’ University of Medicine and Pharmacy, Bucharest, Romania.
    Tsolaki, Magda
    Aristotle University of Thessaloniki, Memory and Dementia Centre, G. Papanicolaore General Hospital, Thessaloniki, Greece.
    Wallin, Åsa K
    Department of Clinical Sciences Malm ̈ o, Clinical Memory Research Unit, Lund University, Sweden.
    Scheltens, Philip
    Department of Neurology and Alzheimer Center, VU University Medical Center, Amsterdam, The Netherlands.
    Verhey, Frans
    Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Visser, Pieter Jelle
    Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands; Department of Neurology and Alzheimer Center, VU University Medical Center, Amsterdam, The Netherlands.
    Association Between Later Life Lifestyle Factors and Alzheimer's Disease Biomarkers in Non-Demented Individuals: A Longitudinal Descriptive Cohort Study2017In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 60, no 4, p. 1387-1395Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Lifestyle factors have been associated with the risk of dementia, but the association with Alzheimer's disease (AD) remains unclear.

    OBJECTIVE: To examine the association between later life lifestyle factors and AD biomarkers (i.e., amyloid-β 1-42 (Aβ42) and tau in cerebrospinal fluid (CSF), and hippocampal volume) in individuals with subjective cognitive decline (SCD) and mild cognitive impairment (MCI). In addition, to examine the effect of later life lifestyle factors on developing AD-type dementia in individuals with MCI.

    METHODS: We selected individuals with SCD (n = 111) and MCI (n = 353) from the DESCRIPA and Kuopio Longitudinal MCI studies. CSF Aβ42 and tau concentrations were assessed with ELISA assay and hippocampal volume with multi-atlas segmentation. Lifestyle was assessed by clinical interview at baseline for: social activity, physical activity, cognitive activity, smoking, alcohol consumption, and sleep. We performed logistic and Cox regression analyses adjusted for study site, age, gender, education, and diagnosis. Prediction for AD-type dementia was performed in individuals with MCI only.

    RESULTS: Later life lifestyle factors were not associated with AD biomarkers or with conversion to AD-type dementia. AD biomarkers were strongly associated with conversion to AD-type dementia, but these relations were not modulated by lifestyle factors. Apolipoprotein E (APOE) genotype did not influence the results.

    CONCLUSIONS: Later life lifestyle factors had no impact on key AD biomarkers in individuals with SCD and MCI or on conversion to AD-type dementia in MCI.

  • 10.
    van Waalwijk van Doorn, Linda J. C.
    et al.
    Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud Alzheimer Centre, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud Alzheimer Centre, Radboud University Medical Center, Nijmegen, The Netherlands .
    Freund-Levi, Yvonne
    Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden; Department of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Verbeek, Marcel M.
    Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud Alzheimer Centre, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud Alzheimer Centre, Radboud University Medical Center, Nijmegen, The Netherlands .
    Improved Cerebrospinal Fluid-Based Discrimination between Alzheimer's Disease Patients and Controls after Correction for Ventricular Volumes2017In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 56, no 2, p. 543-555Article in journal (Refereed)
    Abstract [en]

    Cerebrospinal fluid (CSF) biomarkers may support the diagnosis of Alzheimer's disease (AD). We studied if the diagnostic power of AD CSF biomarker concentrations, i.e., Aβ42, total tau (t-tau), and phosphorylated tau (p-tau), is affected by differences in lateral ventricular volume (VV), using CSF biomarker data and magnetic resonance imaging (MRI) scans of 730 subjects, from 13 European Memory Clinics. We developed a Matlab-algorithm for standardized automated segmentation analysis of T1 weighted MRI scans in SPM8 for determining VV, and computed its ratio with total intracranial volume (TIV) as proxy for total CSF volume. The diagnostic power of CSF biomarkers (and their combination), either corrected for VV/TIV ratio or not, was determined by ROC analysis. CSF Aβ42 levels inversely correlated to VV/TIV in the whole study population (Aβ42: r = -0.28; p < 0.0001). For CSF t-tau and p-tau, this association only reached statistical significance in the combined MCI and AD group (t-tau: r = -0.15; p-tau: r = -0.13; both p < 0.01). Correction for differences in VV/TIV improved the differentiation of AD versus controls based on CSF Aβ42 alone (AUC: 0.75 versus 0.81) or in combination with t-tau (AUC: 0.81 versus 0.91). In conclusion, differences in VV may be an important confounder in interpreting CSF Aβ42 levels.

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