Evidence map›Paper›PMID 27716672›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Tocotrienol-Rich Fraction Modulates Amyloid Pathology and Improves Cognitive Function in AβPP/PS1 Mice.

Nor Faeizah Ibrahim, Daijiro Yanagisawa, Lina Wati Durani, Hamizah Shahirah Hamezah, Hanafi Ahmad Damanhuri, Wan Zurinah Wan Ngah, Mayumi Tsuji, Yuji Kiuchi, Kenjiro Ono, Ikuo Tooyama

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Effect of Vitamin E on Transcriptomic Alterations in Alzheimer's Disease.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

10 authors at 3 institutions in 2 countries.

Nor Faeizah IbrahimMolecular Neuroscience Research Center, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Japan.
Daijiro YanagisawaMolecular Neuroscience Research Center, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Japan.
Lina Wati DuraniMolecular Neuroscience Research Center, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Japan.
Hamizah Shahirah HamezahMolecular Neuroscience Research Center, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Japan.
Hanafi Ahmad DamanhuriDepartment of Biochemistry, Faculty of Medicine, UKMMC, Universiti Kebangsaan Malaysia, Jalan Yaacob Latif, Cheras, Kuala Lumpur, Malaysia.
Wan Zurinah Wan NgahDepartment of Biochemistry, Faculty of Medicine, UKMMC, Universiti Kebangsaan Malaysia, Jalan Yaacob Latif, Cheras, Kuala Lumpur, Malaysia.
Mayumi TsujiDepartment of Pharmacology, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan.
Yuji KiuchiDepartment of Pharmacology, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan.
Kenjiro OnoDepartment of Neurology, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan.
Ikuo TooyamaMolecular Neuroscience Research Center, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Japan.
Shiga University of Medical Science · JPNational University of Malaysia · MYShowa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia. The cardinal neuropathological characteristic of AD is the accumulation of amyloid-β (Aβ) into extracellular plaques that ultimately disrupt neuronal function and lead to neurodegeneration. One possible therapeutic strategy therefore is to prevent Aβ aggregation. Previous studies have suggested that vitamin E analogs slow AD progression in humans. In the present study, we investigated the effects of the tocotrienol-rich fraction (TRF), a mixture of vitamin E analogs from palm oil, on amyloid pathology in vitro and in vivo. TRF treatment dose-dependently inhibited the formation of Aβ fibrils and Aβ oligomers in vitro. Moreover, daily TRF supplementation to AβPPswe/PS1dE9 double transgenic mice for 10 months attenuated Aβ immunoreactive depositions and thioflavin-S-positive fibrillar type plaques in the brain, and eventually improved cognitive function in the novel object recognition test compared with control AβPPswe/PS1dE9 mice. The present result indicates that TRF reduced amyloid pathology and improved cognitive functions, and suggests that TRF is a potential therapeutic agent for AD.

Indexed as

Alzheimer DiseaseAmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAntioxidantsCell Line, TumorCognition DisordersDisease Models, AnimalHumansMiceMice, Inbred C57BLMice, TransgenicMutationNeuroblastomaPeptide FragmentsAmyloidAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorAntioxidantsPeptide FragmentsPresenilin-1TocotrienolsAlzheimer’s diseaseamyloid-βAβPP/PS1 micetocotrienol-rich fractionvitamin E

Identifiers

PMID27716672
PMCPMC5147513
OpenAlexW2527927989

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.