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Review
. 2017 Nov;58(11):2083-2101.
doi: 10.1194/jlr.R076331. Epub 2017 May 20.

Omega-3 fatty acids, lipids, and apoE lipidation in Alzheimer's disease: a rationale for multi-nutrient dementia prevention

Marcus O W Grimm  1 , Daniel M Michaelson  2 , Tobias Hartmann  1
Affiliations
Review

Omega-3 fatty acids, lipids, and apoE lipidation in Alzheimer's disease: a rationale for multi-nutrient dementia prevention

Marcus O W Grimm et al. J Lipid Res. 2017 Nov.

Abstract

In the last decade, it has become obvious that Alzheimer's disease (AD) is closely linked to changes in lipids or lipid metabolism. One of the main pathological hallmarks of AD is amyloid-β (Aβ) deposition. Aβ is derived from sequential proteolytic processing of the amyloid precursor protein (APP). Interestingly, both, the APP and all APP secretases are transmembrane proteins that cleave APP close to and in the lipid bilayer. Moreover, apoE4 has been identified as the most prevalent genetic risk factor for AD. ApoE is the main lipoprotein in the brain, which has an abundant role in the transport of lipids and brain lipid metabolism. Several lipidomic approaches revealed changes in the lipid levels of cerebrospinal fluid or in post mortem AD brains. Here, we review the impact of apoE and lipids in AD, focusing on the major brain lipid classes, sphingomyelin, plasmalogens, gangliosides, sulfatides, DHA, and EPA, as well as on lipid signaling molecules, like ceramide and sphingosine-1-phosphate. As nutritional approaches showed limited beneficial effects in clinical studies, the opportunities of combining different supplements in multi-nutritional approaches are discussed and summarized.

Keywords: amyloid-β; apolipoprotein E; apolipoproteins; ceramide; docosahexaenoic acid; nutrition; sphingomyelin.

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Figures

Fig. 1.
Fig. 1.
Chemical structure of the sphingolipids that are altered in AD.
Fig. 2.
Fig. 2.
Chemical structure of plasmalogens.
Fig. 3.
Fig. 3.
Chemical structure of the FAs, DHA and EPA.
See this image and copyright information in PMC

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