Evidence map›Paper›PMID 33114450›Full record

ReviewMolecules (Basel, Switzerland)2020

Attenuation of Nrf2/Keap1/ARE in Alzheimer's Disease by Plant Secondary Metabolites: A Mechanistic Review.

Sajad Fakhri, Mirko Pesce, Antonia Patruno, Seyed Zachariah Moradi, Amin Iranpanah, Mohammad Hosein Farzaei, Eduardo Sobarzo-Sánchez

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
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  13. Reinforcing Nrf2 Signaling: Help in the Alzheimer's Disease Context.International journal of molecular sciences · 2025
    Review
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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 3 institutions in 4 countries.

Sajad FakhriPharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah 6734667149, Iran.
Mirko PesceDepartment of Medicine and Aging Sciences, University G. d'Annunzio CH-PE, 66100 Chieti, Italy.
Antonia PatrunoDepartment of Medicine and Aging Sciences, University G. d'Annunzio CH-PE, 66100 Chieti, Italy.
Seyed Zachariah MoradiPharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah 6734667149, Iran.ORCID 0000-0003-0579-3495
Amin IranpanahStudent Research Committee, Kermanshah University of Medical Sciences, Kermanshah 6714415153, Iran.
Mohammad Hosein FarzaeiPharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah 6734667149, Iran.ORCID 0000-0001-7081-6521
Eduardo Sobarzo-SánchezLaboratory of Pharmaceutical Chemistry, Department of Organic Chemistry, Faculty of Pharmacy, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain.ORCID 0000-0002-2790-2544
Kermanshah University of Medical Sciences · IRUniversity of Chieti-Pescara · ITUniversidade de Santiago de Compostela · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neuronal/cognitional dysfunction, leading to disability and death. Despite advances in revealing the pathophysiological mechanisms behind AD, no effective treatment has yet been provided. It urges the need for finding novel multi-target agents in combating the complex dysregulated mechanisms in AD. Amongst the dysregulated pathophysiological pathways in AD, oxidative stress seems to play a critical role in the pathogenesis progression of AD, with a dominant role of nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein-1 (Keap1)/antioxidant responsive elements (ARE) pathway. In the present study, a comprehensive review was conducted using the existing electronic databases, including PubMed, Medline, Web of Science, and Scopus, as well as related articles in the field. Nrf2/Keap1/ARE has shown to be the upstream orchestrate of oxidative pathways, which also ameliorates various inflammatory and apoptotic pathways. So, developing multi-target agents with higher efficacy and lower side effects could pave the road in the prevention/management of AD. The plant kingdom is now a great source of natural secondary metabolites in targeting Nrf2/Keap1/ARE. Among natural entities, phenolic compounds, alkaloids, terpene/terpenoids, carotenoids, sulfur-compounds, as well as some other miscellaneous plant-derived compounds have shown promising future accordingly. Prevailing evidence has shown that activating Nrf2/ARE and downstream antioxidant enzymes, as well as inhibiting Keap1 could play hopeful roles in overcoming AD. The current review highlights the neuroprotective effects of plant secondary metabolites through targeting Nrf2/Keap1/ARE and downstream interconnected mediators in combating AD.

Indexed as

AlkaloidsAlzheimer DiseaseAnimalsAntioxidant Response ElementsBiological ProductsCarotenoidsDatabases, PharmaceuticalDrug Evaluation, PreclinicalHumansKelch-Like ECH-Associated Protein 1Neuroprotective AgentsNF-E2-Related Factor 2Oxidative StressPhenolsPlant ExtractsSecondary MetabolismAlkaloidsBiological ProductsCarotenoidsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1Neuroprotective AgentsNFE2L2 protein, humanNF-E2-Related Factor 2PhenolsPlant ExtractsTerpenesAlzheimer’s diseaseantioxidant response elementsKeap1Nrf2oxidative stresspharmacologyphytochemicalssecondary metabolites

Identifiers

PMID33114450
PMCPMC7663041
OpenAlexW3093732257

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.