Evidence map›Paper›PMID 39719518›Full record

ReviewCellular and molecular neurobiology2024

Molecular Signaling Pathways of Quercetin in Alzheimer's Disease: A Promising Arena.

Mansour A Alsaleem, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Ali K Albuhadily, Mohammed Alrouji, Asmaa S A Yassen, Athanasios Alexiou, Marios Papadakis, Gaber El-Saber Batiha

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

9 authors.

Mansour A AlsaleemUnit of Scientific Research, Applied College, Qassim University, Qassim, Saudi Arabia.
Hayder M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ali I Al-GareebDepartment of Clinical Pharmacology and Medicine, Jabir Ibn Hayyan Medical University, Kufa, Iraq.
Ali K AlbuhadilyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Mohammed AlroujiDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Shaqra University, Shaqra, 11961, Saudi Arabia. malrouji@su.edu.sa.
Asmaa S A YassenDepartment of Medicinal Chemistry, Faculty of Pharmacy, Galala University, New Galala City, Suez, 43713, Egypt. asmaa.yassen@gu.edu.eg.ORCID http://orcid.org/0000-0002-7956-9739
Athanasios AlexiouUniversity Centre for Research & Development, Chandigarh University, Chandigarh-Ludhiana Highway, Mohali, Punjab, India.ORCID http://orcid.org/0000-0002-2206-7236
Marios PapadakisUniversity Hospital Witten-Herdecke, University of Witten-Herdecke, Heusnerstrasse 40, 42283, Wuppertal, Germany. drmariospapadakis@gmail.com.
Gaber El-Saber BatihaDepartment of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, AlBeheira, Egypt. gaberbatiha@gmail.com.ORCID http://orcid.org/0000-0002-7817-425X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease characterized by cognitive impairment and memory deficit. Even with extensive research and studies, presently, there is no effective treatment for the management of AD. Besides, most of drugs used in the treatment of AD did not avert the AD neuropathology, and the disease still in a progressive status. For example, acetyl cholinesterase inhibitors are associated with many adverse effects, such as insomnia and nightmares. As well, acetylcholinesterase inhibitors augment cholinergic neurotransmission leading to the development of adverse effects related to high acetylcholine level, such as salivation, rhinorrhea, vomiting, loss of appetite, and seizure. Furthermore, tacrine has poor bioavailability and causes hepatotoxicity. These commonly used drugs do not manage the original causes of AD. For those reasons, natural products were repurposed for the treatment of AD and neurodegenerative diseases. It has been shown that phytochemicals produce neuroprotective effects against the development and progression of neurodegenerative diseases by different mechanisms, including antioxidant and anti-inflammatory effects. Quercetin (QCN) has been reported to exert an effective neuroprotective effect against AD and other neurodegenerative diseases by lessening oxidative stress. In this review, electronic databases such as PubMed, Scopus, and Web of Science were searched for possible relevant studies and article linking the effect of QCN on AD. Findings from this review highlighted that many studies highlighted different mechanistic signaling pathways regarding the neuroprotective effect of QCN in AD. Nevertheless, the precise molecular mechanism of QCN in AD was not completely clarified. Consequently, this review aims to discuss the molecular mechanism of QCN in AD.

Indexed as

Alzheimer DiseaseQuercetinSignal TransductionAnimalsAntioxidantsHumansNeuroprotective AgentsOxidative StressAntioxidantsNeuroprotective AgentsQuercetinAlzheimer’s diseaseMolecular mechanismNeurodegenerative diseasesNeuroprotective effectOxidative stressQuercetin

Identifiers

PMID39719518
PMCPMC11668837

What Socratic holds

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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 Socratic graph.