Evidence map›Paper›PMID 39563011›Full record

ArticleCNS neuroscience & therapeutics2024

9-Methylfascaplysin Prevents Neuroinflammation and Synaptic Damage via Cell-Specific Inhibition of Kinases in APP/PS1 Transgenic Mice.

Jingyang Le, Chenglong Xia, Jiayi Xu, Jinhan Cai, Chenwei Hu, Yu Bai, Huiyue Chen, Wenni Rong, Yujie Jiang, Xinming Wu and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Sunitinib attenuates secondary injury via the regulation of peri-hematomal microglia at the acute phase of intracerebral hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. Article
  3. Review
  4. Article
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

20 authors.

Jingyang LeTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Chenglong XiaKey Laboratory of Advanced Mass Spectrometry and Molecular Analysis of Zhejiang Province, School of Materials Science and Chemical Engineering, Ningbo University, Zhejiang, China.
Jiayi XuTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Jinhan CaiTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Chenwei HuTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Yu BaiCollege of Food and Pharmaceutical Sciences, Ningbo University, Zhejiang, China.
Huiyue ChenTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Wenni RongTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Yujie JiangTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Xinming WuCollege of Biotechnology, Tianjin University of Science & Technology; Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin Key Laboratory of Industrial Microbiology, Tianjin, China.
Yongmei LiSchool Infirmary, Ningbo University, Zhejiang, China.
Qiyao WangTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
C Benjamin NamanDepartment of Science and Conservation, San Diego Botanic Garden, California, USA.
Hua WeiNingbo College of Health Sciences, Zhejiang, China.
Jili ZhangTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Hao LiuTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Xiaowei ChenTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.
Fufeng LiuCollege of Biotechnology, Tianjin University of Science & Technology; Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin Key Laboratory of Industrial Microbiology, Tianjin, China.
Hongze LiangKey Laboratory of Advanced Mass Spectrometry and Molecular Analysis of Zhejiang Province, School of Materials Science and Chemical Engineering, Ningbo University, Zhejiang, China.
Wei CuiTranslational Medicine Center of Pain, Emotion and Cognition, Health Science Center, Ningbo University, Zhejiang, China.

Funding

Applied Research Project on Nonprofit Technology of Ningbo 2021S088Applied Research Project on Nonprofit Technology of Zhejiang Province LGF20C090002K. C. Wong Magna Fund in Ningbo UniversityLiDakSum Marine Biopharmaceutical Development FundNational Natural Science Foundation of China 82101354National Natural Science Foundation of China 82271443Ningbo Science and Technology Development Special Fund 2024Z191Ningbo Top Medical and Health Research Program 2022020304One Health Interdisciplinary Research Project in Ningbo University HY202410
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a leading neurodegenerative disorder without effective treatments. The nonlinear dynamic nature of AD pathophysiology suggested that multiple pharmacological actions of anti-AD drugs should be elucidated. 9-Methylfascaplysin (9-MF) was previously designed and synthesized as a novel anti-AD candidate. METHODS AND

resultsIn this study, 9-MF at low concentrations significantly prevented cognitive impairments with similar efficacy as donepezil in APP/PS1 transgenic mice. In addition, 9-MF potently reduced β-amyloid (Aβ)-associated neuroinflammation and tau-associated synaptic damage in vivo. 9-MF-regulated microglia-specific differentially phosphorylated proteins (DPPs) were mainly enriched in neuroinflammation, while 9-MF-regulated neuron-specific DPPs were enriched in synaptic regulation, as revealed by a quantitative phosphoproteomic approach. A phosphoproteome-kinome algorithm further identified that rho-associated coiled-coil kinase 2 (ROCK2) and glycogen synthase kinase 3β (GSK3β) ranked high in 9-MF-downregulated kinase perturbations. 9-MF possessed high affinities for ROCK2 and GSK3β, which was confirmed by in vitro kinase activity assay. The protective effects of 9-MF were abolished by ROCK2 knockdown in Aβ-treated BV2 microglial cells, and by GSK3β knockdown in glyceraldehyde-treated SH-SY5Y neuronal cells, respectively.

conclusionsAll these results supported that 9-MF produced anti-AD effects via cell-specific inhibition of ROCK2 and GSK3β in microglia and neurons, respectively.

Indexed as

Amyloid beta-Protein PrecursorMice, TransgenicNeuroinflammatory DiseasesPresenilin-1Alzheimer DiseaseAnimalsGlycogen Synthase Kinase 3 betaHumansMaleMiceMice, Inbred C57BLNeuroprotective Agentsrho-Associated KinasesSynapsesAmyloid beta-Protein PrecursorGlycogen Synthase Kinase 3 betaGsk3b protein, mouseNeuroprotective AgentsPresenilin-1rho-Associated KinasesRock2 protein, mouse9‐MethylfascaplysinAlzheimer's diseasechemical‐proteomicsGSK3βomics‐based approachesphosphoproteomicsROCK2

Identifiers

PMID39563011
PMCPMC11576489

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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.