Evidence map›Paper›PMID 29579687›Full record

ArticleNeurobiology of aging2018

Deuterated polyunsaturated fatty acids reduce brain lipid peroxidation and hippocampal amyloid β-peptide levels, without discernable behavioral effects in an APP/PS1 mutant transgenic mouse model of Alzheimer's disease.

Sophia M Raefsky, Ran Furman, Ginger Milne, Erik Pollock, Paul Axelsen, Mark P Mattson, Mikhail S Shchepinov

Abstract read
In one paragraph

Article in Neurobiology of aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 85 citations in OpenAlex.

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  6. Journal of the American Chemical Society · 2025
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  12. Identification of novel FRedox biology · 2024
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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

7 authors at 6 institutions in 1 country.

Sophia M RaefskyLaboratory of Neurosciences, National Institute on Aging, Baltimore, MD.
Ran FurmanDepartments of Pharmacology, Biochemistry and Biophysics, and Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA.
Ginger MilneEicosanoid Core Laboratory, Vanderbilt University Medical Center, Nashville, TN.
Erik PollockStable Isotope Laboratory, University of Arkansas, Fayetteville, AR.
Paul AxelsenDepartments of Pharmacology, Biochemistry and Biophysics, and Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA.
Mark P MattsonLaboratory of Neurosciences, National Institute on Aging, Baltimore, MD; Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD. Electronic address: mark.mattson@nih.gov.
Mikhail S ShchepinovRetrotope, Los Altos, CA.
University of Pennsylvania · USJohns Hopkins University · USNational Institute on Aging · USRetrotope (United States) · USUniversity of Arkansas at Fayetteville · USVanderbilt University Medical Center · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Dietary Modification Of Brain Aging And Neurodegenerative DisordersZIAAG000315 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$5.0M
Intramural NIH HHS ZIA AG000312Intramural NIH HHS ZIA AG000315NIEHS NIH HHS P30 ES013508
6 · The paper itself

Abstract

Alzheimer's disease (AD) involves progressive deposition of amyloid β-peptide (Aβ), synapse loss, and neuronal death, which occur in brain regions critical for learning and memory. Considerable evidence suggests that lipid peroxidation contributes to synaptic dysfunction and neuronal degeneration, both upstream and downstream of Aβ pathology. Recent findings suggest that lipid peroxidation can be inhibited by replacement of polyunsaturated fatty acids (PUFA) with isotope-reinforced (deuterated) PUFA (D-PUFA), and that D-PUFA can protect neurons in experimental models of Parkinson's disease. Here, we determined whether dietary D-PUFA would ameliorate Aβ pathology and/or cognitive deficits in a mouse model of AD (amyloid precursor protein/presenilin 1 double mutant transgenic mice). The D-PUFA diet did not ameliorate spatial learning and memory deficits in the AD mice. Compared to mice fed an hydrogenated-PUFA control diet, those fed D-PUFA for 5 months exhibited high levels of incorporation of deuterium into arachidonic acid and docosahexaenoic acid, and reduced concentrations of lipid peroxidation products (F2 isoprostanes and neuroprostanes), in the brain tissues. Concentrations of Aβ40 and Aβ38 in the hippocampus were significantly lower, with a trend to reduced concentrations of Aβ42, in mice fed D-PUFA compared to those fed hydrogenated-PUFA. We conclude that a D-PUFA diet reduces the brain tissue concentrations of both arachidonic acid and docosahexaenoic acid oxidation products, as well as the concentration of Aβs.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsDepression, ChemicalDeuteriumDietary SupplementsDisease Models, AnimalFatty Acids, UnsaturatedFemaleHippocampusLipid PeroxidationMaleMemoryMice, TransgenicSpatial LearningAmyloid beta-PeptidesDeuteriumFatty Acids, UnsaturatedAmyloidHippocampusHydroxynonenalLearning and memoryLipid peroxidationPUFA

Identifiers

PMID29579687
PMCPMC5924637
OpenAlexW2792346211

What OpenQuestion holds

Textmetadata
LicenceTDM
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.