Evidence map›Paper›PMID 42507320›Full record

ArticleCNS neuroscience & therapeutics2026

Betulinaldehyde Ameliorates Aβ-Induced Neurotoxicity and Cognitive Deficits by Modulating the eEF2K/eEF2 Pathway.

Chaoqun Wang, Xiaohe Han, Yali Lin, Yan Pan, Qiuping Miao, Yaping Wang, Shu-Qin Wang, Zhu Zhang, Luyao Wang, Zhi-Ri Tang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CNS neuroscience & therapeutics, 2026. 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
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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.

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

16 authors.

Chaoqun WangState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.
Xiaohe HanState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.
Yali LinState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.
Yan PanDepartment of Biology, Hong Kong Baptist University, Kowloon, Hong Kong SAR, China.
Qiuping MiaoState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.
Yaping WangDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Jinan University, Guangzhou, China.ORCID 0000-0002-1753-0863
Shu-Qin WangState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.
Zhu ZhangTeaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Kowloon, Hong Kong SAR, China.ORCID 0000-0001-5009-4680
Luyao WangLaw Sau Fai Institute for Advancing Translational Medicine in Bone & Joint Diseases (TMBJ), Hong Kong Baptist University, Kowloon, Hong Kong SAR, China.
Zhi-Ri TangSchool of Intelligent Systems Science and Engineering, Jinan University, Guangzhou, China.ORCID 0000-0002-0900-6500
Yinghui PengState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.
Ken Kin-Lam YungDepartment of Science and Environmental Studies, The Education University of Hong Kong, Hong Kong, Hong Kong SAR, China.
Nan MaState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.
Dan LuDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Shiqing ZhangState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.ORCID 0000-0002-0785-5461
Lei ShiState Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou, China.ORCID 0000-0001-8695-3432

Funding

Guangdong Basic and Applied Basic Research Foundation 2022B1515130007Guangdong Basic and Applied Basic Research Foundation 2023A1515030012Guangdong Basic and Applied Basic Research Foundation 2023B1515040015International Science and Technology Projects of Guangdong Province 2023A0505050121National Key Research and Development Program of China 2022YFA1104900National Natural Science Foundation of China 82371175National Natural Science Foundation of China U24A20804The Brain Science and Brain-like Intelligence Technology-National Science and Technology Major Project 2022ZD0214400The Research Project of Guangdong Provincial Bureau of Traditional Chinese Medicine 20261073The Science and Technology Projects in Guangzhou 202102070001
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD), the most common form of dementia, remains without effective therapies. Dysregulated eukaryotic elongation factor 2 kinase/eukaryotic elongation factor 2 (eEF2K/eEF2) pathway leads to aberrant protein synthesis and impaired neuronal function in AD, positioning this axis as a promising therapeutic target. However, effective pharmacological modulators of eEF2K/eEF2 remain limited. Betulinaldehyde (Betu), an active ingredient derived from traditional Chinese medicine, remains to be thoroughly evaluated as a potential neuroprotective agent. PURPOSE: This study aims to investigate the therapeutic effects of Betu on AD and determine whether its activities are mediated through the eEF2K/eEF2 pathway.

methodsNeuronal cell models were used to assess the effects of Betu on β-amyloid 42 (Aβ

resultsBetu significantly ameliorated the Aβ

conclusionThese findings demonstrate that Betu protects against Aβ

Indexed as

Amyloid beta-PeptidesCognition DisordersElongation Factor 2 KinaseNeuroprotective AgentsPeptide FragmentsTriterpenesAnimalsHumansMiceMice, Inbred C57BLNeuronsSignal TransductionAmyloid beta-Peptidesamyloid beta-protein (1-42)Eef2k protein, mouseElongation Factor 2 KinaseNeuroprotective AgentsPeptide FragmentsTriterpenesAlzheimer's diseaseAβ42‐induced neurotoxicitybetulinaldehydeeEF2K/eEF2neuroprotection

Identifiers

PMID42507320
PMCPMC13404250

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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.