Evidence map›Paper›PMID 31905173›Full record

ArticleAging2020

Activation of α7 nAChR by PNU-282987 improves synaptic and cognitive functions through restoring the expression of synaptic-associated proteins and the CaM-CaMKII-CREB signaling pathway.

Xiao-Ling Wang, Yu-Xin Deng, Yu-Mei Gao, Yang-Ting Dong, Fan Wang, Zhi-Zhong Guan, Wei Hong, Xiao-Lan Qi

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  10. Human restrictedFrontiers in neuroscience · 2024
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  18. Effects of nicotine on DARPP-32 and CaMKII signaling relevant to addiction.Advances in pharmacology (San Diego, Calif.) · 2021
    Review
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  20. 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

8 authors at 2 institutions in 1 country.

Xiao-Ling WangKey Laboratory of Endemic and Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, P.R. China.
Yu-Xin DengKey Laboratory of Endemic and Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, P.R. China.
Yu-Mei GaoKey Laboratory of Endemic and Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, P.R. China.
Yang-Ting DongKey Laboratory of Endemic and Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, P.R. China.
Fan WangDepartment of Neurosurgery, Affiliated Hospital of Guizhou Medical University , Guiyang 550004, P.R. China.
Zhi-Zhong GuanKey Laboratory of Endemic and Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, P.R. China.
Wei HongKey Laboratory of Endemic and Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, P.R. China.
Xiao-Lan QiKey Laboratory of Endemic and Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, P.R. China.
Guiyang Medical University · CNAffiliated Hospital of Guizhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ligands of nicotinic acetylcholine receptors (nAChRs) are widely considered as potential therapeutic agents. The present study used primary hippocampus cells and APPswe/PSEN1dE9 double-transgenic mice models to study the possible therapeutic effect and underlying mechanism of the specific activation of α7 nAChR by PNU-282987 in the pathogenesis of Alzheimer's disease. The results indicated that activation of α7 nAChR attenuated the Aβ-induced cell apoptosis, decreased the deposition of Aβ, increased the expression of synaptic-associated proteins, and maintained synaptic morphology. Furthermore, in the APP/PS1_DT mice model, activation of α7 nAChR attenuated Aβ-induced synaptic loss, reduced the deposition of Aβ in the hippocampus, maintained the integral structure of hippocampus-derived synapse, and activated the calmodulin (CaM)-calmodulin-dependent protein kinase II (CaMKII)-cAMP response element-binding protein signaling pathway by upregulation of its key signaling proteins. In addition, activation of α7 nAChR improved the learning and memory abilities of the APP/PS1_DT mice. Collectively, the activation of α7 nAChR by PNU-282987 attenuated the toxic effect of Aβ

Indexed as

Signal Transductionalpha7 Nicotinic Acetylcholine ReceptorAlzheimer DiseaseAmyloid beta-PeptidesAnimalsApoptosisBenzamidesBridged Bicyclo CompoundsCalcium-Calmodulin-Dependent Protein Kinase Type 2CognitionCyclic AMP Response Element-Binding ProteinDisease Models, AnimalHippocampusLearningMemoryNeuronsalpha7 Nicotinic Acetylcholine ReceptorAmyloid beta-PeptidesBenzamidesBridged Bicyclo CompoundsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cyclic AMP Response Element-Binding ProteinNicotinic AgonistsPNU-282987Alzheimer’s diseaseCaM-CaMKII-CREB signaling pathwaysynapseα7 nAChRβ-amyloid peptide

Identifiers

PMID31905173
PMCPMC6977648
OpenAlexW2999345105

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.