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Effects of supplementation with omega-3 fatty acids on oxidative stress and inflammation in patients with Alzheimer's disease: the OmegAD study
Section of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet and Department of Geriatrics Karolinska University Hospital Stockholm, Sweden.ORCID iD: 0000-0001-6863-6679
Division of Haematology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
Division of Geriatrics, Uppsala University, Uppsala, Sweden; Chaire d'Excellence Program, Department of Biochemistry, Molecular Biology and Nutrition, Universite d'Auvergne, Clermont-Ferrand, France.
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2014 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 42, no 3, p. 823-831Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
IOS Press, 2014. Vol. 42, no 3, p. 823-831
Keywords [en]
F2-isoprostane, Alzheimer's disease, eicosanoids, inflammation, lipids, omega-3 fatty acids, oxidative stress, prostaglandin F2α
National Category
Neurology Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:oru:diva-74053DOI: 10.3233/JAD-132042ISI: 000342237000011PubMedID: 24934544Scopus ID: 2-s2.0-84907155927OAI: oai:DiVA.org:oru-74053DiVA, id: diva2:1313964
Note

Funding agencies:

Stockholm County Council and Karolinska Institutet (20110263, 20110604, 20110604)

Funds of Capio

Demensförbundet

Gamla Tjänarinnor

Swedish Alzheimer Foundation

Gun och Bertil Stohnes Stiftelse

Swedish Society of Physicians

Lion's Sweden

Pronova Biocare A/S, Lysaker, Norway

Available from: 2019-05-07 Created: 2019-05-07 Last updated: 2019-06-18Bibliographically approved

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Freund-Levi, Yvonne

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