Evidence map›Paper›PMID 32556702›Full record

ArticleNeurochemical research2020

A Novel Compound YS-5-23 Exhibits Neuroprotective Effect by Reducing β-Site Amyloid Precursor Protein Cleaving Enzyme 1's Expression and H

Chen Cheng, Nan Zheng, Deyang Sun, Weishuo Fang, Lingling Zheng, Weihong Song, Jian Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 53% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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 4 institutions in 1 country.

Chen ChengHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, Hubei, China.
Nan ZhengCollege of Bioengineering, Wuhan Polytechnic, Wuhan, 430074, Hubei, China.
Deyang SunState Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Science & Peking Union Medical College (CAMS&PUMC), 2A Nan Wei Road, Beijing, 100050, China.
Weishuo FangState Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Science & Peking Union Medical College (CAMS&PUMC), 2A Nan Wei Road, Beijing, 100050, China.
Lingling ZhengChongqing City Key Lab of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, and Ministry of Education Key Lab of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Weihong SongChongqing City Key Lab of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, and Ministry of Education Key Lab of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Jian HuangHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, Hubei, China. jianhuang@whu.edu.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNChongqing Medical University · CNWuhan University · CNWuhan Polytechnic University · CN

Funding

National Natural Science Foundation of China 31371331National Natural Science Foundation of China 31870786National Natural Science Foundation of China 81273406
6 · The paper itself

Abstract

The abnormally accumulated amyloid-β (Aβ) and oxidative stress contribute to the initiation and progression of Alzheimer's disease (AD). β-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the rate-limiting enzyme for the production of Aβ. Furthermore, Aβ was reported to increase oxidative stress; then the overproduced oxidative stress continues to increase the expression and activity of BACE1. Consequently, inhibition of both BACE1 and oxidative stress is a better strategy for AD therapy compared with those one-target treatment methods. In the present study, our novel small molecule YS-5-23 was proved to possess both of the activities. Specifically, we found that YS-5-23 reduces BACE1's expression in both SH-SY5Y and Swedish mutated amyloid precursor protein (APP) overexpressed HEK293 cells, and it can also suppress BACE1's expression induced by H

Indexed as

Amyloid Precursor Protein SecretasesAntioxidantsAspartic Acid EndopeptidasesCell Line, TumorCoumaric AcidsFlavonesHEK293 CellsHumansHydrogen PeroxideMembrane Potential, MitochondrialMitochondriaNeuroprotective AgentsOxidative StressPhosphatidylinositol 3-KinasesProtease InhibitorsProto-Oncogene Proteins c-aktAmyloid Precursor Protein SecretasesAntioxidantsAspartic Acid EndopeptidasesBACE1 protein, humanCoumaric AcidsFlavonesHydrogen PeroxideNeuroprotective AgentsPhosphatidylinositol 3-KinasesProtease InhibitorsProto-Oncogene Proteins c-aktAlzheimer’s diseaseBACE1Oxidative stressPI3K/Akt

Identifiers

PMID32556702
OpenAlexW3036846186

What OpenQuestion holds

Textmetadata
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.