Evidence map›Paper›PMID 25471398›Full record

ReviewMedical principles and practice : international journal of the Kuwait University, Health Science Centre2015

Amyloid-beta: a crucial factor in Alzheimer's disease.

Saeed Sadigh-Eteghad, Babak Sabermarouf, Alireza Majdi, Mahnaz Talebi, Mehdi Farhoudi, Javad Mahmoudi

Registry-linked trialOpen access · diamondAbstract readReview
In one paragraph

Review in Medical principles and practice : international journal of the Kuwait University, Health Science Centre, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03451760 (Feru-guard), which is not on this map. Cited by 252 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
252citing papers in PubMed, 4 pooled it
10.9field-weighted citation impact, top 1% 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.

NCT03451760 phase2unknown statusnot on this mapstarted 2018, after this paper: background citation

Feru-guard (Ferulic Acid and Angelica Archangelica Extract) for Behavioral Symptoms in Dementia

TypeinterventionalSponsorGlovia Co., Ltd.Ran2018 to 2019Enrolled70ConditionsBehavioral and Psychiatric Symptoms of DementiaArmsFeru-guard 100M, Feru-guard 100M Placebo
3 · Its place in the literature

Who cites it

252 citing papers in PubMed, 4 syntheses or guidelines pooled it, 518 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Gut microbes · 2026
    Article
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  9. Review
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  11. Review
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  17. Chrysin Ameliorated Neurochemical and Behavioural Changes Mediated By Combined Exposure of Interleukin-17 A With Amyloid BetaJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  18. Article
  19. Review
  20. Article

192 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Saeed Sadigh-EteghadNeurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Babak Sabermarouf
Alireza Majdi
Mahnaz Talebi
Mehdi Farhoudi
Javad Mahmoudi
Tabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent form of dementia which affects people older than 60 years of age. In AD, the dysregulation of the amyloid-beta (Aβ) level leads to the appearance of senile plaques which contain Aβ depositions. Aβ is a complex biological molecule which interacts with many types of receptors and/or forms insoluble assemblies and, eventually, its nonphysiological depositions alternate with the normal neuronal conditions. In this situation, AD signs appear and the patients experience marked cognitional disabilities. In general, intellect, social skills, personality, and memory are influenced by this disease and, in the long run, it leads to a reduction in quality of life and life expectancy. Due to the pivotal role of Aβ in the pathobiology of AD, a great deal of effort has been made to reveal its exact role in neuronal dysfunctions and to finding efficacious therapeutic strategies against its adverse neuronal outcomes. Hence, the determination of its different molecular assemblies and the mechanisms underlying its pathological effects are of interest. In the present paper, some of the well-established structural forms of Aβ, its interactions with various receptors and possible molecular and cellular mechanisms underlying its neurotoxicity are discussed. In addition, several Aβ-based rodent models of AD are reviewed.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersDisease Models, AnimalHippocampusHumansMicePlaque, AmyloidPrionsAmyloid beta-PeptidesBiomarkersPrions

Identifiers

PMID25471398
PMCPMC5588216
OpenAlexW2027009370

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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.