Evidence map›Paper›PMID 33980877›Full record

ArticleScientific reports2021

Dietary cis-9, trans-11-conjugated linoleic acid reduces amyloid β-protein accumulation and upregulates anti-inflammatory cytokines in an Alzheimer's disease mouse model.

Yu Fujita, Kuniyuki Kano, Shigenobu Kishino, Toshihiro Nagao, Xuefeng Shen, Chiharu Sato, Hatsune Hatakeyama, Yume Ota, Sho Niibori, Ayako Nomura and 11 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. The omega-3 postbioticFrontiers in cellular and infection microbiology · 2024
    Article
  11. Review
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

21 authors at 7 institutions in 1 country.

Yu FujitaDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Kuniyuki KanoLaboratory of Molecular and Cellular Biochemistry, Graduates School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
Shigenobu KishinoDivision of Applied Life Sciences, Graduate School of Agriculture, Kyoto University, Sakyo-ku, Kyoto, Japan.
Toshihiro NagaoOsaka Research Institute of Industrial Science and Technology, Morinomiya Center, Joto-ku, Osaka, Japan.
Xuefeng ShenDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Chiharu SatoDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Hatsune HatakeyamaDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Yume OtaDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Sho NiiboriDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Ayako NomuraDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Kota KikuchiDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan.
Wataru YasunoInstitute for Biomedical Sciences, Library, Iwate Medical University, Nishitokuta, Yahaba-cho, Shiwa-gun, Iwate, Japan.
Sho TakatoriLaboratory of Neuropathology and Neuroscience, Graduates School of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Kazunori KikuchiLaboratory of Neuropathology and Neuroscience, Graduates School of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Yoshitake SanoDepartment of Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science, Noda, Japan.
Taisuke TomitaLaboratory of Neuropathology and Neuroscience, Graduates School of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Toshiharu SuzukiLaboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Junken AokiLaboratory of Molecular and Cellular Biochemistry, Graduates School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
Kun ZouDepartment of Biochemistry, School of Medicine, Nagoya City University, Nagoya, Aichi, Japan.
Shunji NatoriGraduates School of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan. natori@e-mail.jp.
Hiroto KomanoDivision of Neuroscience, School of Pharmacy, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan. hirotokomano@gmail.com.
Iwate Medical University · JPThe University of Tokyo · JPHokkaido University · JPKyoto University · JPNagoya City University · JPOsaka Research Institute of Industrial Science and Technology · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Conjugated linoleic acid (CLA) is an isomer of linoleic acid (LA). The predominant dietary CLA is cis-9, trans-11-CLA (c-9, t-11-CLA), which constitutes up to ~ 90% of total CLA and is thought to be responsible for the positive health benefits associated with CLA. However, the effects of c-9, t-11-CLA on Alzheimer's disease (AD) remain to be elucidated. In this study, we investigated the effect of dietary intake of c-9, t-11-CLA on the pathogenesis of an AD mouse model. We found that c-9, t-11-CLA diet-fed AD model mice significantly exhibited (1) a decrease in amyloid-β protein (Aβ) levels in the hippocampus, (2) an increase in the number of microglia, and (3) an increase in the number of astrocytes expressing the anti-inflammatory cytokines, interleukin-10 and 19 (IL-10, IL-19), with no change in the total number of astrocytes. In addition, liquid chromatography-tandem mass spectrometry (LC-MS/MS) and gas chromatographic analysis revealed that the levels of lysophosphatidylcholine (LPC) containing c-9, t-11-CLA (CLA-LPC) and free c-9, t-11-CLA were significantly increased in the brain of c-9, t-11-CLA diet-fed mice. Thus, dietary c-9, t-11-CLA entered the brain and appeared to exhibit beneficial effects on AD, including a decrease in Aβ levels and suppression of inflammation.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCytokinesDietary Fats, UnsaturatedDisease Models, AnimalHumansLinoleic Acids, ConjugatedMiceMice, Inbred C57BLAmyloid beta-Peptidescis-9, trans-11-conjugated linoleic acidCytokinesDietary Fats, UnsaturatedLinoleic Acids, Conjugated

Identifiers

PMID33980877
PMCPMC8115273
OpenAlexW3160481399

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.