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Omega-3 fatty acids enhance phagocytosis of Alzheimer's disease-related amyloid-β42 by human microglia and decrease inflammatory markers
Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
Division of Neurodegeneration, Department of Neurobiology, Care Sciences & Society, Karolinska Institutet, Stockholm, Sweden.
Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
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2013 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 35, no 4, p. 697-713Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
IOS Press, 2013. Vol. 35, no 4, p. 697-713
Keywords [en]
Amyloid, brain-derived neurotrophic factor, cytokine, DHA, EPA, interleukin, M1, M2, resolution
National Category
Neurology
Identifiers
URN: urn:nbn:se:oru:diva-74155DOI: 10.3233/JAD-130131ISI: 000319345300005PubMedID: 23481688Scopus ID: 2-s2.0-84878838444OAI: oai:DiVA.org:oru-74155DiVA, id: diva2:1314551
Funder
Swedish Research Council, 072194Knut and Alice Wallenberg FoundationThe Karolinska Institutet's Research FoundationStiftelsen Gamla TjänarinnorStockholm County Council
Note

Funding Agencies:

Swedish Brain Power

Swedish Brain Foundation

Swedish Alzheimer Foundation  

Gun och Bertil Stohnes stiftelse  

Petrus och Augusta Hedlunds Stiftelse 

Available from: 2019-05-09 Created: 2019-05-09 Last updated: 2019-06-18Bibliographically approved

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Freund-Levi, Yvonne

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