Evidence map›Paper›PMID 40220255›Full record

ArticleNeurochemical research2025

OAB-14 Attenuated Glymphatic System Disorder, Neuroinflammation and Dyskinesia in Parkinson's Disease Model Mice Induced by Rotenone.

Xinyu Zhao, Ruolin Cao, Xiaoyi Tian, Peng Liu, Danyang Liu, Xin Yu, Zhonghui Zheng, Guo-Liang Chen, Libo Zou

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Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
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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

9 authors.

Xinyu ZhaoDepartment of Pharmacology, Life Science and Biopharmaceutics School, Shenyang Pharmaceutical University, Shenyang, Liaoning, 110016, PR China.
Ruolin CaoDepartment of Pharmacology, Life Science and Biopharmaceutics School, Shenyang Pharmaceutical University, Shenyang, Liaoning, 110016, PR China.
Xiaoyi TianDepartment of Pharmacology, Life Science and Biopharmaceutics School, Shenyang Pharmaceutical University, Shenyang, Liaoning, 110016, PR China.
Peng LiuDepartment of Pharmacology, Life Science and Biopharmaceutics School, Shenyang Pharmaceutical University, Shenyang, Liaoning, 110016, PR China.
Danyang LiuDepartment of Pharmacology, Life Science and Biopharmaceutics School, Shenyang Pharmaceutical University, Shenyang, Liaoning, 110016, PR China.
Xin YuSchool of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Ministry of Education, Yantai University, Yantai, 264005, P.R. China.
Zhonghui ZhengShandong Xinhua Pharmaceutical Co., Ltd, Zibo, Shandong, 255086, PR China.
Guo-Liang ChenKey Laboratory of Structure-Based Drugs Design & Discovery of Ministry of Education, School of Pharmaceutical Engineering, Shenyang Pharmaceutical University, Shenyang, Liaoning, 110016, PR China. spucgl@163.com.
Libo ZouKey Laboratory of Structure-Based Drugs Design & Discovery of Ministry of Education, School of Pharmaceutical Engineering, Shenyang Pharmaceutical University, Shenyang, Liaoning, 110016, PR China. libozou@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's Disease (PD) is a neurodegenerative disorder characterized by the pathological accumulation of alpha-synuclein (α-syn) in the neuronal cell bodies of the substantia nigra. The glymphatic system within the Central Nervous System (CNS) is responsible for clearing metabolic waste and abnormal proteins and its dysfunction may significantly contribute to the pathogenesis of PD. Our previous study showed that OAB-14, the novel small molecular compound, showed a great potential effect in APP/PS1 transgenic mice. Given the similarities in the pathogenesis of PD and Alzheimer's disease (AD), it is pertinent to explore the therapeutic potential of OAB-14 in the context of PD. This study utilized a rotenone-induced PD mice model to evaluate the effects of oral administration of OAB-14, and its underlying mechanisms. Here we confirmed the neuroprotective effect and motor improvement of OAB-14 in rotenone-induced PD model mice. Our research has shown that OAB-14 is capable of enhancing the glymphatic system function by promoting the influx and efflux of the CSF tracers to the brain and deep cervical lymph nodes, respectively, to promote the clearance of α-syn. In addition, OAB-14 could down-regulate MyD88, NF-kB (Ser 536) phosphorylation, and TLR4 to reduce glial cell activation; and down-regulate cleaved-caspase1, NLRP3, ASC, IL-1β, IL-6, IL-18, TNF-α, and IL-10 to reduce the expression of inflammatory vesicles and pro-inflammatory factors, and to reduce neuronal oxidative stress. In summary, OAB-14 may promote the clearance of brain α-syn through the glial lymphatic system, inhibit the α-syn/TLR4/NF-κB/NLRP3 inflammatory pathway, and improve movement disorders.

Indexed as

DyskinesiasGlymphatic SystemNeuroinflammatory DiseasesNeuroprotective AgentsParkinsonian Disordersalpha-SynucleinAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLParkinson DiseaseRotenonealpha-SynucleinNeuroprotective AgentsRotenoneGlymphatic SystemInflammatoryOAB-14Parkinson's Disease

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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.