Evidence map›Paper›PMID 30596401›Full record

ArticleCNS neuroscience & therapeutics2018

Novel synthetic chalcone-coumarin hybrid for Aβ aggregation reduction, antioxidation, and neuroprotection.

Shin-Ying Lee, Ya-Jen Chiu, Shu-Mei Yang, Chiung-Mei Chen, Chin-Chang Huang, Guey-Jen Lee-Chen, Wenwei Lin, Kuo-Hsuan Chang

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

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  15. Using ΔK280 TauBiomolecules · 2023
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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

8 authors at 2 institutions in 1 country.

Shin-Ying LeeDepartment of Life Science, National Taiwan Normal University, Taipei, Taiwan.
Ya-Jen ChiuDepartment of Life Science, National Taiwan Normal University, Taipei, Taiwan.
Shu-Mei YangDepartment of Chemistry, National Taiwan Normal University, Taipei, Taiwan.
Chiung-Mei ChenDepartment of Neurology, Chang Gung Memorial Hospital-Linkou Medical Center, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Chin-Chang HuangDepartment of Neurology, Chang Gung Memorial Hospital-Linkou Medical Center, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Guey-Jen Lee-ChenDepartment of Life Science, National Taiwan Normal University, Taipei, Taiwan.ORCID 0000-0003-4818-9917
Wenwei LinDepartment of Chemistry, National Taiwan Normal University, Taipei, Taiwan.ORCID 0000-0002-1121-072X
Kuo-Hsuan ChangDepartment of Neurology, Chang Gung Memorial Hospital-Linkou Medical Center, Chang Gung University College of Medicine, Taoyuan, Taiwan.ORCID 0000-0003-4972-9823
National Taiwan Normal University · TWChang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAggregation of misfolded amyloid β (Aβ) in senile plaques causes oxidative stress and neuronal death in Alzheimer's disease (AD). Compounds possessing antiaggregation and antioxidant properties are promising candidate compounds for AD treatment.

methodsWe examined the potential of synthetic derivatives of licochalcone A and coumarin for inhibiting Aβ aggregation, scavenging reactive oxygen species (ROS), and providing neuroprotection by using biochemical assays and Tet-On Aβ-GFP 293/SH-SY5Y cell models for AD.

resultsAmong test compounds, LM-031, a novel chalcone-coumarin hybrid, inhibited Aβ aggregation and scavenged free oxygen radicals. LM-031 markedly reduced Aβ misfolding and ROS as well as promoted neurite outgrowth and inhibited acetylcholinesterase in Tet-On Aβ-GFP 293/SH-SY5Y cells. Mechanistic studies showed upregulation of the HSPB1 chaperone, NRF2/NQO1/GCLC pathway, and CREB/BDNF/BCL2 pathway. Decreased neurite outgrowth upon the induction of Aβ-GFP was rescued by LM-031, which was counteracted by knockdown of HSPB1, NRF2, or CREB.

conclusionTaken together, these findings demonstrate that LM-031 exhibited antiaggregation, antioxidant, and neuroprotective effects against Aβ toxicity by enhancing HSPB1 and the NRF2-related antioxidant pathway as well as by activating the CREB-dependent survival and antiapoptosis pathway. These results imply that LM-031 may be a new therapeutic compound for AD.

Indexed as

AcetylcholinesteraseAmyloid beta-PeptidesAntioxidantsCell Line, TumorChalconeCoumarinsDose-Response Relationship, DrugGene Expression RegulationGreen Fluorescent ProteinsHumansInhibitory Concentration 50NeuroblastomaNeuronal OutgrowthProtein AggregatesReactive Oxygen SpeciesRNA InterferenceAcetylcholinesteraseAmyloid beta-PeptidesAntioxidantsChalconecoumarinCoumarinsGreen Fluorescent ProteinsProtein AggregatesReactive Oxygen SpeciesRNA, MessengerAlzheimer’s diseaseantioxidationAβ aggregation reductionchalcone‐coumarin hybridneuroprotectiontherapeutics

Identifiers

PMID30596401
PMCPMC6490010
OpenAlexW2890134706

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.