Evidence map›Paper›PMID 25333200›Full record

ReviewNutrients2014

Fatty acid metabolism in carriers of apolipoprotein E epsilon 4 allele: is it contributing to higher risk of cognitive decline and coronary heart disease?

Raphaël Chouinard-Watkins, Mélanie Plourde

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nutrients, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 6 pooled it
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 6 syntheses or guidelines pooled it, 68 citations in OpenAlex.

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  18. Nutritional metabolism and cerebral bioenergetics in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Review
  19. Contribution of Genetic Polymorphisms in Human Health.International journal of environmental research and public health · 2023
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Raphaël Chouinard-WatkinsResearch Center on Aging, Health and Social Services Centre-University Institute of Geriatrics of Sherbrooke, Department of medicine, Université de Sherbrooke, 1036 Belvédère Sud, Sherbrooke, J1H 4C4, Canada. raphael.chouinard-watkins@usherbrooke.ca.
Mélanie PlourdeResearch Center on Aging, Health and Social Services Centre-University Institute of Geriatrics of Sherbrooke, Department of medicine, Université de Sherbrooke, 1036 Belvédère Sud, Sherbrooke, J1H 4C4, Canada. Melanie.plourde2@usherbrooke.ca.
Health and Social Services Centre University Institute of Geriatrics of Sherbrooke · CA

Funding

Canadian Institutes of Health Research MOP 119454
6 · The paper itself

Abstract

Apolipoprotein E (ApoE) is a protein playing a pivotal role in lipid homeostasis since it regulates cholesterol, triglyceride and phospholipid metabolism in the blood and the brain. APOE gene regulates the expression of this protein and has three different alleles: ε2, ε3 and ε4. Carrying an APOE4 allele is recognised as a genetic risk factor of late-onset Alzheimer's disease (LOAD) and coronary heart disease (CHD). Consuming fatty fish, rich in long chain omega-3 fatty acids (LC omega-3), seems to be associated with risk reduction of developing LOAD and CHD but this link seems not to hold in APOE4 carriers, at least in LOAD. In CHD trials, APOE4 carriers supplemented with LC omega-3 were categorized as differential responders to the treatment with regards to CHD risk markers. This is potentially because fatty acid metabolism is disturbed in APOE4 carriers compared to the non-carriers. More specifically, homeostasis of LC omega-3 is disrupted in carriers of APOE4 allele and this is potentially because they β-oxidize more LC omega-3 than the non-carriers. Therefore, there is a potential shift in fatty acid selection for β-oxidation towards LC omega-3 which are usually highly preserved for incorporation into cell membranes.

Indexed as

Dietary SupplementsAllelesAlzheimer DiseaseAnimalsApolipoprotein E4Cognition DisordersCoronary DiseaseFatty Acids, Omega-3FishesGenetic Predisposition to DiseaseHeterozygoteHomeostasisHumansLipid MetabolismOxidation-ReductionRisk FactorsApolipoprotein E4Fatty Acids, Omega-3

Identifiers

PMID25333200
PMCPMC4210928
OpenAlexW2079783485

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.