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Your search keyword '"Yvonne Freund-Levi"' showing total 4 results
Start Over Author "Yvonne Freund-Levi" Publisher elsevier
4 results on '"Yvonne Freund-Levi"'

1. Effects of n-3 FA supplementation on the release of proresolving lipid mediators by blood mononuclear cells: the OmegAD study[S]

Author

Xiuzhe Wang, Erik Hjorth, Inger Vedin, Maria Eriksdotter, Yvonne Freund-Levi, Lars-Olof Wahlund, Tommy Cederholm, Jan Palmblad, and Marianne Schultzberg

Subjects
amyloid β, Alzheimer's disease, clinical trials, docosahexaenoic acid, fish oil, inflammation, Biochemistry, QD415-436
Abstract

Specialized proresolving mediators (SPMs) induce resolution of inflammation. SPMs are derivatives of n-3 and n-6 PUFAs and may mediate their beneficial effects. It is unknown whether supplementation with PUFAs influences the production of SPMs. Alzheimer's disease (AD) is associated with brain inflammation and reduced levels of SPMs. The OmegAD study is a randomized, double-blind, and placebo-controlled clinical trial on AD patients, in which placebo or a supplement of 1.7 g DHA and 0.6 g EPA was taken daily for 6 months. Plasma levels of arachidonic acid decreased, and DHA and EPA levels increased after 6 months of n-3 FA treatment. Peripheral blood mononuclear cells (PBMCs) were obtained before and after the trial. Analysis of the culture medium of PBMCs incubated with amyloid-β 1–40 showed unchanged levels of the SPMs lipoxin A4 and resolvin D1 in the group supplemented with n-3 FAs, whereas a decrease was seen in the placebo group. The changes in SPMs showed correspondence to cognitive changes. Changes in the levels of SPMs were positively correlated to changes in transthyretin. We conclude that supplementation with n-3 PUFAs for 6 months prevented a reduction in SPMs released from PBMCs of AD patients, which was associated with changes in cognitive function.

Published
2015
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2. Reduced prostaglandin F2α release from blood mononuclear leukocytes after oral supplementation of ω3 fatty acids: the OmegAD study

Author

Inger Vedin, Tommy Cederholm, Yvonne Freund-Levi, Hans Basun, Erik Hjorth, Gerd Faxén Irving, Maria Eriksdotter-Jönhagen, Marianne Schultzberg, Lars-Olof Wahlund, and Jan Palmblad

Subjects
DHA, EPA, LPS, Omega-3 fatty acid, PBMC, PGF, Biochemistry, QD415-436
Abstract

Omega-3 fatty acids, e.g., dokosahexaenoic acid (DHA) and eikosapentaenoic acid (EPA), ameliorate inflammatory reactions by various mechanisms, but the role of prostaglandins remains unclear. Our aim was to determine if dietary supplementation with a DHA-rich fish oil influenced the release of PGF2α from peripheral blood mononuclear cells (PBMC). In the OmegAD study, 174 Alzheimer disease patients received either 1.7 g DHA plus 0.6 g EPA or a placebo daily for six months. PBMCs from the 21 (9 on fish oil and 12 on placebo) first-randomized patients were stimulated with either lipopolysaccharide (LPS) or phytohemagglutinin (PHA) before and after 6 months. Our results showed that plasma concentrations of DHA and EPA increased significantly at 6 months in the omega-3 group. PGF2α release from LPS- (but not from PHA-) stimulated PBMC was significantly diminished in this group; no change was noted in the placebo group. PGF2α changes correlated inversely with changes in plasma DHA and EPA. Decreased IL-6 and IL-1β levels correlated with decreased PGF2α levels. The stimulus-specific PGF2α 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.

Published
2010
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3. Prevalence of the apolipoprotein E E4 allele in amyloid B positive subjects across the spectrum of Alzheimer's disease

Author

Dong Young Lee, Vincent Camus, Sudesh Prabhakar, Anne M. Fagan, Aleksandra Klimkowicz-Mrowiec, Julius Popp, Frans R.J. Verhey, Victor L. Villemagne, David J. Brooks, Susan M. Landau, Kewei Chen, Johannes Kornhuber, Duk L. Na, Linda J C van Waalwijk van Doorn, Mony J. de Leon, Ann D. Cohen, Charlotte E. Teunissen, Eloy Rodríguez-Rodríguez, Erik Stomrud, Philip Scheltens, Wiesje M. van der Flier, Adrian Ivanoiu, Anders Wallin, Eckart Rüther, Adam S. Fleisher, Isabel Santana, Ramesh Kandimalla, Tormod Fladby, Åsa K. Wallin, Peter Johannsen, Stefan Förster, Sang W. Seo, Gaël Chételat, Koen Van Laere, Ina S. Almdahl, Mark M. Mintun, Dag Aarsland, Sanna-Kaisa Herukka, Harald Hampel, Magda Tsolaki, Henrik Zetterberg, Kristian Steen Frederiksen, John C. Morris, David A. Wolk, Marie Sarazin, Hilkka Soininen, Catherine M. Roe, Sebastiaan Engelborghs, Juha O. Rinne, Hanne Struyfs, Daniel Alcolea, Pieter Jelle Visser, Oliver Peters, Willemijn J. Jansen, Alberto Lleó, Bart N.M. van Berckel, Kiran Dip Gill, Arto Nordlund, Jens Wiltfang, Kaj Blennow, Timo Grimmer, Johannes Schröder, Pauline Aalten, Colin Groot, Pascual Sánchez-Juan, Jan Marcusson, Inês Baldeiras, Mark A. van Buchem, Niklas Mattsson, Christopher C. Rowe, Rik Ossenkoppele, Wolfgang Maier, Agneta Nordberg, Rik Vandenberghe, William E. Klunk, Hanne M. Møllergård, José Luis Molinuevo, Stephanie J.B. Vos, Olymbia Gkatzima, Alexander Drzezga, Oskar Hansson, Lorena Rami, Giovanni B. Frisoni, Karen M. Rodrigue, Olga Meulenbroek, Barbara Mroczko, Marcel M. Verbeek, Juan Fortea, Gil D. Rabinovici, William J. Jagust, Yvonne Freund-Levi, Luiza Spiru, Gunhild Waldemar, Catarina R. Oliveira, Enrica Cavedo, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Psychiatrie & Neuropsychologie, MUMC+: MA Med Staf Spec Psychiatrie (9), Frisoni, Giovanni, Popp, Julius, Neurology, Amsterdam Neuroscience - Neurodegeneration, Laboratory Medicine, Radiology and nuclear medicine, APH - Personalized Medicine, and APH - Methodology

Subjects
0301 basic medicine, Apolipoprotein E, Male, NATIONAL INSTITUTE, Neurology, Epidemiology, Apolipoprotein E4, LONGITUDINAL COHORT, Disease, metabolism [Cognitive Dysfunction], ddc:616.89, 0302 clinical medicine, Prevalence, Geographical location, genetics [Apolipoprotein E4], APOE GENOTYPE, Health Policy, GLUCOSE-METABOLISM, CEREBROSPINAL-FLUID BIOMARKERS, Alzheimer's disease, Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3], 3. Good health, Europe, Psychiatry and Mental health, cerebrospinal fluid [Biomarkers], Biomarker (medicine), lipids (amino acids, peptides, and proteins), Female, Sex, ASSOCIATION WORKGROUPS, metabolism [Alzheimer Disease], APOE, medicine.medical_specialty, Amyloid, CSF BIOMARKERS, metabolism [Amyloid beta-Peptides], CSF, ta3112, Education, 03 medical and health sciences, Cellular and Molecular Neuroscience, Age, Developmental Neuroscience, Alzheimer Disease, Internal medicine, mental disorders, medicine, Dementia, Humans, Cognitive Dysfunction, ddc:610, Allele, OLDER-ADULTS, Biology, Alleles, Aged, Amyloid beta-Peptides, business.industry, Mild cognitive impairment, medicine.disease, nervous system diseases, 030104 developmental biology, Endocrinology, PET, Positron-Emission Tomography, ddc:618.97, Subjective cognitive decline, DIAGNOSTIC GUIDELINES, Human medicine, Neurology (clinical), Geriatrics and Gerontology, business, 030217 neurology & neurosurgery, Biomarkers
Abstract

Introduction: Apolipoprotein E (APOE) epsilon 4 is the major genetic risk factor for Alzheimer's disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid beta(A beta) pathology. Methods: We included 3451 A beta+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE epsilon 4 prevalence in relation to age, sex, education, and geographical location. Results: The APOE epsilon 4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in A beta+ cognitively normal and A beta+ mild cognitive impairment (P

Published
2018

4. Effects of n-3 FA supplementation on the release of proresolving lipid mediators by blood mononuclear cells: the OmegAD study[S]

Author

Maria Eriksdotter, Jan Palmblad, Yvonne Freund-Levi, Inger Vedin, Xiuzhe Wang, Tommy Cederholm, Marianne Schultzberg, Erik Hjorth, and Lars-Olof Wahlund

Subjects
Male, medicine.medical_specialty, Inflammation, QD415-436, Biology, Placebo, Peripheral blood mononuclear cell, fish oil, Biochemistry, chemistry.chemical_compound, Cognition, Endocrinology, Double-Blind Method, Alzheimer Disease, Fatty Acids, Omega-6, Internal medicine, Fatty Acids, Omega-3, medicine, Humans, Cells, Cultured, Aged, Aged, 80 and over, Lipoxin, clinical trials, Amyloid beta-Peptides, Cell Biology, Alzheimer's disease, docosahexaenoic acid, Fish oil, Peptide Fragments, chemistry, Docosahexaenoic acid, inflammation, Immunology, Leukocytes, Mononuclear, amyloid β, Female, Arachidonic acid, lipids (amino acids, peptides, and proteins), sense organs, Inflammation Mediators, medicine.symptom, Patient-Oriented and Epidemiological Research, Resolvin
Abstract

Specialized proresolving mediators (SPMs) induce resolution of inflammation. SPMs are derivatives of n-3 and n-6 PUFAs and may mediate their beneficial effects. It is unknown whether supplementation with PUFAs influences the production of SPMs. Alzheimer’s disease (AD) is associated with brain inflammation and reduced levels of SPMs. The OmegAD study is a randomized, double-blind, and placebo-controlled clinical trial on AD patients, in which placebo or a supplement of 1.7 g DHA and 0.6 g EPA was taken daily for 6 months. Plasma levels of arachidonic acid decreased, and DHA and EPA levels increased after 6 months of n-3 FA treatment. Peripheral blood mononuclear cells (PBMCs) were obtained before and after the trial. Analysis of the culture medium of PBMCs incubated with amyloid-β 1–40 showed unchanged levels of the SPMs lipoxin A4 and resolvin D1 in the group supplemented with n-3 FAs, whereas a decrease was seen in the placebo group. The changes in SPMs showed correspondence to cognitive changes. Changes in the levels of SPMs were positively correlated to changes in transthyretin. We conclude that supplementation with n-3 PUFAs for 6 months prevented a reduction in SPMs released from PBMCs of AD patients, which was associated with changes in cognitive function.

Published
2015

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