Evidence map›Paper›PMID 31291354›Full record

ArticlePloS one2019

Characterization of the unique In Vitro effects of unsaturated fatty acids on the formation of amyloid β fibrils.

Miki Eto, Tadafumi Hashimoto, Takao Shimizu, Takeshi Iwatsubo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Elucidation of molecular mechanisms by which amyloid βBiochimica et biophysica acta. Molecular and cell biology of lipids · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Article
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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

4 authors at 2 institutions in 1 country.

Miki EtoDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tadafumi HashimotoDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Takao ShimizuDepartment of Lipid Signaling, National Center for Global Health and Medicine, Tokyo, Japan.
Takeshi IwatsuboDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-1160-8129
National Center for Global Health and Medicine · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulation of amyloid ß (Aß) peptides, the major component of amyloid fibrils in senile plaques, is one of the main causes of Alzheimer's disease. Docosahexaenoic acid (DHA) is a fatty acid abundant in the brain, and is reported to have protective effects against Alzheimer's disease, although the mechanistic effects of DHA against Alzheimer's pathophysiology remain unclear. Because dietary supplementation of DHA in Aß precursor protein transgenic mice ameliorates Aß pathology and behavioral deficits, we hypothesize that DHA may affect the fibrillization and deposition of Aß. Here we studied the effect of different types of fatty acids on Aß fibril formation by in vitro Aß fibrillization assay. Formation of amyloid fibrils consists of two steps, i.e., the initial nucleation phase and the following elongation phase. We found that unsaturated fatty acids, especially DHA, accelerated the formation of Aß fibrils with a unique short and curved morphology in its nucleation phase, which did not elongate further into the long and straight, mature Aß fibrils. Addition of DHA afterwards did not modify the morphology of the mature Aß(1-40) fibrils. The short and curved Aß fibrils formed in the presence of DHA did not facilitate the elongation phase of Aß fibril formation, suggesting that DHA promotes the formation of "off-pathway" conformers of Aß. Our study unravels a possible mechanism of how DHA acts protectively against the pathophysiology of Alzheimer's disease.

Indexed as

Alzheimer DiseaseAmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloidosisAnimalsBrainDietary SupplementsDisease Models, AnimalDocosahexaenoic AcidsFatty Acids, UnsaturatedHumansMiceMice, TransgenicPeptide FragmentsAmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorDocosahexaenoic AcidsFatty Acids, UnsaturatedPeptide Fragments

Identifiers

PMID31291354
PMCPMC6619765
OpenAlexW2960775483

What OpenQuestion holds

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LicenceCC BY
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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.