Evidence map›Paper›PMID 36221038›Full record

ArticlePsychopharmacology2022

Rose Bengal inhibits β-amyloid oligomers-induced tau hyperphosphorylation via acting on Akt and CDK5 kinases.

Chen-Ye Mou, Yan-Fei Xie, Jia-Xin Wei, Qi-Yao Wang, Jing-Yang Le, Yong-Jie Bao, Pan-Pan Zhang, Yue-Chun Mao, Xing-Han Huang, Han-Bo Pan and 6 more

Abstract read
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In one paragraph

Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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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

16 authors at 1 institution in 1 country.

Chen-Ye MouThe Affiliated Hospital of Medical School, Ningbo University, Ningbo, 315211, China.
Yan-Fei XieTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Jia-Xin WeiThe Affiliated Hospital of Medical School, Ningbo University, Ningbo, 315211, China.
Qi-Yao WangTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Jing-Yang LeTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Yong-Jie BaoTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Pan-Pan ZhangTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Yue-Chun MaoTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Xing-Han HuangTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Han-Bo PanTranslational Medicine Center of Pain, Emotion and Cognition, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
C Benjamin NamanLi Dak Sum Yip Yio Chin Kenneth Li Marine Biopharmaceutical Research Center, School of Food and Pharmaceutical Sciences, Ningbo University, Ningbo, 315211, China.
Lin LiuThe Affiliated Hospital of Medical School, Ningbo University, Ningbo, 315211, China.
Hong-Ze LiangSchool of Materials Science and Chemical Engineering, Ningbo University, Ningbo, 315211, China.
Xiang WuThe Affiliated Hospital of Medical School, Ningbo University, Ningbo, 315211, China.
Jia XuThe Affiliated Hospital of Medical School, Ningbo University, Ningbo, 315211, China.
Wei CuiThe Affiliated Hospital of Medical School, Ningbo University, Ningbo, 315211, China. cuiwei@nbu.edu.cn.
Ningbo University · CN

Funding

Major program of Ningbo Science and Technology Innovation 2025 2019B10067Medical Health Science and Technology Project of Zhejiang Provincial Health Commission 2019RC266Medical Health Science and Technology Project of Zhejiang Provincial Health Commission 2021KY1043National Natural Science Foundation of China 81870853Natural Science Foundation of Ningbo 2013A610247Natural Science Foundation of Ningbo 202003N4247Natural Science Foundation of Zhejiang Province LY19H25001Natural Science Foundation of Zhejiang Province LY21H090002Ningbo medical science and technology project 2019Y16The Affiliated Hospital of Medical School of Ningbo University Youth Talent Cultivation Program FYQM-LC-202002
6 · The paper itself

Abstract

rationaleTau hyperphosphorylation and aggregation is considered as a main pathological mechanism underlying Alzheimer's disease (AD). Rose Bengal (RB) is a synthetic dye used for disease diagnosis, which was reported to inhibit tau toxicity via inhibiting tau aggregation in Drosophila. However, it was unknown if RB could produce anti-AD effects in rodents.

objectivesThe research aimed to investigate if and how RB could prevent β-amyloid (Aβ) oligomers-induced tau hyperphosphorylation in rodents. METHODS AND

resultsRB was tested in vitro (0.3-1 μM) and prevented Aβ oligomers-induced tau hyperphosphorylation in PC12 cells. Moreover, RB (10-30 mg/kg, i.p.) effectively attenuated cognitive impairments induced by Aβ oligomers in mice. Western blotting analysis demonstrated that RB significantly increased the expression of pSer473-Akt, pSer9-glycogen synthase kinase-3β (GSK3β) and reduced the expression of cyclin-dependent kinase 5 (CDK5) both in vitro and in vivo. Molecular docking analysis suggested that RB might directly interact with GSK3β and CDK5 by acting on ATP binding sites. Gene Ontology enrichment analysis indicated that RB might act on protein phosphorylation pathways to inhibit tau hyperphosphorylation.

conclusionsRB was shown to inhibit tau neurotoxicity at least partially via inhibiting the activity of GSK3β and CDK5, which is a novel neuroprotective mechanism besides the inhibition of tau aggregation. As tau hyperphosphorylation is an important target for AD therapy, this study also provided support for investigating the drug repurposing of RB as an anti-AD drug candidate.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAdenosine TriphosphateAnimalsCyclin-Dependent Kinase 5Glycogen Synthase Kinase 3 betaMiceMolecular Docking SimulationPhosphorylationProto-Oncogene Proteins c-aktRatsRose Bengaltau ProteinsAdenosine TriphosphateAmyloid beta-PeptidesCdk5 protein, ratCyclin-Dependent Kinase 5Glycogen Synthase Kinase 3 betaProto-Oncogene Proteins c-aktRose Bengaltau ProteinsAlzheimer’s diseaseCDK5GSK3βRose BengalTau

Identifiers

PMID36221038
OpenAlexW4304588168

What OpenQuestion holds

Textmetadata
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Registered trials

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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.