uu.seUppsala University Publications
Change search
ReferencesLink to record
Permanent link

Direct link
Omega-3 Fatty Acids Enhance Phagocytosis of Alzheimer's Disease-Related Amyloid-beta(42) by Human Microglia and Decrease Inflammatory Markers
Show others and affiliations
2013 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, Vol. 35, no 4, 697-713 p.Article in journal (Refereed) Published
Abstract [en]

The use of supplements withomega-3 (omega 3) 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 omega 3 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 omega 3 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-beta(A beta), 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 A beta(42). Phagocytosis of A beta(42) 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 A beta(42). Phagocytosis of A beta(42) was performed by microglia with a predominance of M2 markers. EPA increased the levels of BDNF in the culture medium. The levels of TNF-alpha 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 A beta(42), 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
2013. Vol. 35, no 4, 697-713 p.
Keyword [en]
Amyloid, brain-derived neurotrophic factor, cytokine, DHA, EPA, interleukin, M1, M2, resolution
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-203369DOI: 10.3233/JAD-130131ISI: 000319345300005OAI: oai:DiVA.org:uu-203369DiVA: diva2:636293
Available from: 2013-07-09 Created: 2013-07-09 Last updated: 2013-07-12Bibliographically approved

Open Access in DiVA

fulltext(542 kB)474 downloads
File information
File name FULLTEXT01.pdfFile size 542 kBChecksum SHA-512
Type fulltextMimetype application/pdf

Other links

Publisher's full text

Search in DiVA

By author/editor
Cederholm, TommyBasun, Hans
By organisation
Clinical Nutrition and MetabolismGeriatrics
In the same journal
Journal of Alzheimer's Disease
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar
Total: 474 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 310 hits
ReferencesLink to record
Permanent link

Direct link