Triple-Target Inhibition of Cholinesterase, Amyloid Aggregation, and GSK3β to Ameliorate Cognitive Deficits and Neuropathology in the Triple-Transgenic Mouse Model of Alzheimer's Disease.

Junqiu He, Shan Sun, Hongfeng Wang, Zheng Ying, Kin Yip Tam

Abstract read

In one paragraph

Article in Neuroscience bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

1 citing paper in PubMed.

Targeting the BACE1-GSK-3β Signaling Axis in Alzheimer's Disease: From Molecular Crosstalk to Nanotechnology-Based Translational Strategies.Molecular neurobiology · 2026
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

5 authors.

Junqiu He *Faculty of Health Sciences, University of Macau, Taipa, Macau SAR, China.

Shan Sun *Faculty of Health Sciences, University of Macau, Taipa, Macau SAR, China.

Hongfeng WangCollege of Pharmaceutical Sciences, Soochow University, Suzhou, 215127, China. wanghongfeng@suda.edu.cn.ORCID http://orcid.org/0000-0003-4909-2260

Zheng YingCollege of Pharmaceutical Sciences, Soochow University, Suzhou, 215127, China. zheng.ying@suda.edu.cn.ORCID http://orcid.org/0000-0002-1099-0509

Kin Yip TamFaculty of Health Sciences, University of Macau, Taipa, Macau SAR, China. kintam@um.edu.mo.ORCID http://orcid.org/0000-0001-5507-8524

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) poses one of the most urgent medical challenges in the 21st century as it affects millions of people. Unfortunately, the etiopathogenesis of AD is not yet fully understood and the current pharmacotherapy options are somewhat limited. Here, we report a novel inhibitor, Compound 44, for targeting cholinesterases, amyloid-β (Aβ) aggregation, and glycogen synthase kinase 3β (GSK-3β) simultaneously with the aim of achieving symptomatic relief and disease modification in AD therapy. We found that Compound 44 had good inhibitory effects on all intended targets with IC

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCholinesterase InhibitorsCognitive DysfunctionGlycogen Synthase Kinase 3 betaAnimalsAutophagyDisease Models, AnimalHumansMiceMice, TransgenicNeuroprotective AgentsAmyloid beta-PeptidesCholinesterase InhibitorsGlycogen Synthase Kinase 3 betaNeuroprotective AgentsAlzheimer’s diseaseAmyloid-β aggregationAutophagyCholinesterasesGSK-3βMulti-targeted inhibitor

Identifiers

PMID39907971

DOI10.1007/s12264-025-01354-y

PMCPMC12014999

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.