Evidence map›Paper›PMID 28934273›Full record

ArticlePloS one2017

Novel derivative of Paeonol, Paeononlsilatie sodium, alleviates behavioral damage and hippocampal dendritic injury in Alzheimer's disease concurrent with cofilin1/phosphorylated-cofilin1 and RAC1/CDC42 alterations in rats.

Fei Han, Ting-Ting Zhuang, Jing-Jing Chen, Xiu-Ling Zhu, Ya-Fei Cai, Ya-Ping Lu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Research in pharmaceutical sciences · 2020
    Article
  8. Role of Cofilin in Alzheimer's Disease.Frontiers in cell and developmental biology · 2020
    Review
  9. The Role of ADF/Cofilin in Synaptic Physiology and Alzheimer's Disease.Frontiers in cell and developmental biology · 2020
    Review
  10. Synaptotoxicity in Alzheimer's Disease Involved a Dysregulation of Actin Cytoskeleton Dynamics through Cofilin 1 Phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  11. 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

6 authors at 1 institution in 1 country.

Fei HanCollege of Life Science, Anhui Normal University, Wuhu, China.
Ting-Ting ZhuangCollege of Life Science, Anhui Normal University, Wuhu, China.
Jing-Jing ChenCollege of Life Science, Anhui Normal University, Wuhu, China.
Xiu-Ling ZhuCollege of Life Science, Anhui Normal University, Wuhu, China.
Ya-Fei CaiCollege of Life Science, Anhui Normal University, Wuhu, China.
Ya-Ping LuCollege of Life Science, Anhui Normal University, Wuhu, China.
Anhui Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a typical hippocampal amnesia and the most common senile dementia. Many studies suggest that cognitive impairments are more closely correlated with synaptic loss than the burden of amyloid deposits in AD progression. To date, there is no effective treatment for this disease. Paeonol has been widely employed in traditional Chinese medicine. This compound improves learning behavior in an animal model; however, the mechanism remains unclear. In this study, Paeononlsilatie sodium (Pa), a derivative of Paeonol, attenuated D-galactose (D-gal) and AlCl3-induced behavioral damages in rats based on evaluations of the open field test (OFT), elevated plus maze test (EPMT), and Morris water maze test (MWMT). Pa increased the dendritic complexity and the density of dendritic spines. Correlation analysis indicated that morphological changes in neuronal dendrites are closely correlated with behavioral changes. Pa treatment reduced the production of Aβ, affected the phosphorylation and redistribution of cofilin1 and inhibited rod-like formation in hippocampal neurons. The induction of D-gal and AlCl3 promoted the expression of RAC1/CDC42 expression; however, the tendency of gene expression was inhibited by pretreatment with Pa. Taken together, our results suggest that Pa may represent a novel therapeutic agent for the improvement of cognitive and emotional behaviors and dendritic morphology in an AD animal model.

Indexed as

AcetophenonesAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAtrophycdc42 GTP-Binding ProteinCofilin 1DendritesDisease Models, AnimalDrug Evaluation, PreclinicalGalactoseHippocampusMaleMaze LearningNeuroprotective AgentsPeptide FragmentsAcetophenonesAmyloid beta-Peptidesamyloid beta-protein (1-42)cdc42 GTP-Binding ProteinCfl1 protein, ratCofilin 1GalactoseMapt protein, ratNeuroprotective AgentsPeptide Fragmentsrac1 GTP-Binding ProteinRac1 protein, ratsodium paeonol sulfatetau Proteins

Identifiers

PMID28934273
PMCPMC5608314
OpenAlexW2758170679

What OpenQuestion holds

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LicenceCC BY
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.