Evidence map›Paper›PMID 31819374›Full record

ArticleDrug design, development and therapy2019

Neuroprotective Effect of S-trans, Trans-farnesylthiosalicylic Acid via Inhibition of RAS/ERK Pathway for the Treatment of Alzheimer's Disease.

Xiang Wang, Yu Wang, Yiyi Zhu, Luxia Yan, Liandong Zhao

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  2. Neurotrophic Effects ofInternational journal of molecular sciences · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Apoptosis in Alzheimer's disease: insight into the signaling pathways and therapeutic avenues.Apoptosis : an international journal on programmed cell death · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
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

5 authors at 2 institutions in 1 country.

Xiang WangDepartment of Neurology, Xuzhou Medical University Affiliated Hospital of Huaian, Huai'an, Jiangsu Province 223002, People's Republic of China.
Yu WangDepartment of Neurology, The Fourth Affiliated Hospital of Nanjing Medical University, Nanjing Pukou Hospital, Nanjing, Jiangsu 210000, People's Republic of China.ORCID 0000-0002-8725-2440
Yiyi ZhuDepartment of Neurology, Xuzhou Medical University Affiliated Hospital of Huaian, Huai'an, Jiangsu Province 223002, People's Republic of China.ORCID 0000-0001-5125-7664
Luxia YanDepartment of Neurology, Xuzhou Medical University Affiliated Hospital of Huaian, Huai'an, Jiangsu Province 223002, People's Republic of China.ORCID 0000-0002-0689-4362
Liandong ZhaoDepartment of Neurology, Xuzhou Medical University Affiliated Hospital of Huaian, Huai'an, Jiangsu Province 223002, People's Republic of China.ORCID 0000-0003-1171-807X
Xuzhou Medical College · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD), a leading cause of dementia, becomes a serious health issue for individuals and society around the world. AD is a neurodegenerative disease characterized by the deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFT) and the loss of large numbers of neurons. To date, there is no effective treatment for AD, and thus, to enhance neurogenesis in the AD brain may be a therapeutic strategy. RAS signaling pathway involves in synaptic plasticity and memory formation, which is overexpressed in brains with AD. This study used Aβ MATERIALS AND

methodsAD model mice were manufactured through intracerebroventricular injection of Aβ

resultsThe results demonstrated that FTS could prevent Aβ

conclusionIn conclusion, these findings suggest that FTS as a RAS inhibitor could be a potential therapeutic agent for the treatment of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimalDoublecortin ProteinExtracellular Signal-Regulated MAP KinasesFarnesolInjections, IntraperitonealMaleMAP Kinase Signaling SystemMaze LearningMiceMice, Inbred ICRMolecular StructureNeuroprotective Agentsras ProteinsAmyloid beta-PeptidesDcx protein, mouseDoublecortin ProteinExtracellular Signal-Regulated MAP KinasesFarnesolfarnesylthiosalicylic acidNeuroprotective Agentsras ProteinsSalicylatesAlzheimer’s diseaseamyloid-βneurogenesissignaling pathwayspatial cognitionS-transtrans-farnesylthiosalicylic acid

Identifiers

PMID31819374
PMCPMC6890185
OpenAlexW2991504277

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.