Abstract
Epidemiological studies suggest a protective role of omega-3 poly-unsaturated fatty acids (n-3 PUFA) against Alzheimers disease (AD). However, most intervention studies of supplementation with n-3 PUFA have yielded disappointing results. One reason for such discordant results may result from inadequate targeting of individuals who might benefit from the supplementation, in particular because of their genetic susceptibility to AD. The 4 allele of the apolipoprotein E gene (ApoE) is a genetic risk factor for late-onset AD. ApoE plays a key role in the transport of cholesterol and other lipids involved in brain composition and functioning. The action of n-3 PUFA on the aging brain might therefore differ according to ApoE polymorphism. The aim of this review is to examine the interaction between dietary fatty acids and ApoE genotype on the risk for AD. Carriers of the 4 allele tend to be the most responsive to changes in dietary fat and cholesterol. Conversely, several epidemiological studies suggest a protective effect of long-chain n-3 PUFA on cognitive decline only in those who do not carry the 4 but with inconsistent results. An intervention study showed that only non-carriers had increased concentrations of long-chain n-3 PUFA in response to supplementation. The mechanisms underlying this gene-by-diet interaction on AD risk may involve impaired fatty acids and cholesterol transport, altered metabolism of n-3 PUFA, glucose or ketones, or modification of other risk factors of AD in 4 carriers. Further research is needed to explain the differential effect of n-3 PUFA on AD according to ApoE genotype
Keywords: Alzheimer's disease, apolipoprotein E, fatty acids, omega 3, nutrition, dementia, ApoE polymorphism, Caucasian homozygotes, glutathion peroxidase
Current Alzheimer Research
Title: Dietary Omega 3 Polyunsaturated Fatty Acids and Alzheimers Disease: Interaction with Apolipoprotein E Genotype
Volume: 8 Issue: 5
Author(s): P. Barberger-Gateau, C. Samieri, C. Feart and M. Plourde
Affiliation:
Keywords: Alzheimer's disease, apolipoprotein E, fatty acids, omega 3, nutrition, dementia, ApoE polymorphism, Caucasian homozygotes, glutathion peroxidase
Abstract: Epidemiological studies suggest a protective role of omega-3 poly-unsaturated fatty acids (n-3 PUFA) against Alzheimers disease (AD). However, most intervention studies of supplementation with n-3 PUFA have yielded disappointing results. One reason for such discordant results may result from inadequate targeting of individuals who might benefit from the supplementation, in particular because of their genetic susceptibility to AD. The 4 allele of the apolipoprotein E gene (ApoE) is a genetic risk factor for late-onset AD. ApoE plays a key role in the transport of cholesterol and other lipids involved in brain composition and functioning. The action of n-3 PUFA on the aging brain might therefore differ according to ApoE polymorphism. The aim of this review is to examine the interaction between dietary fatty acids and ApoE genotype on the risk for AD. Carriers of the 4 allele tend to be the most responsive to changes in dietary fat and cholesterol. Conversely, several epidemiological studies suggest a protective effect of long-chain n-3 PUFA on cognitive decline only in those who do not carry the 4 but with inconsistent results. An intervention study showed that only non-carriers had increased concentrations of long-chain n-3 PUFA in response to supplementation. The mechanisms underlying this gene-by-diet interaction on AD risk may involve impaired fatty acids and cholesterol transport, altered metabolism of n-3 PUFA, glucose or ketones, or modification of other risk factors of AD in 4 carriers. Further research is needed to explain the differential effect of n-3 PUFA on AD according to ApoE genotype
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Barberger-Gateau P., Samieri C., Feart C. and Plourde M., Dietary Omega 3 Polyunsaturated Fatty Acids and Alzheimers Disease: Interaction with Apolipoprotein E Genotype, Current Alzheimer Research 2011; 8 (5) . https://dx.doi.org/10.2174/156720511796391926
DOI https://dx.doi.org/10.2174/156720511796391926 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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