Evidence map›Paper›PMID 32424108›Full record

ArticleAging2020

Clioquinol improves motor and non-motor deficits in MPTP-induced monkey model of Parkinson's disease through AKT/mTOR pathway.

Liangqin Shi, Chao Huang, Qihui Luo, Yu Xia, Wentao Liu, Wen Zeng, Anchun Cheng, Riyi Shi, Chen Zhengli

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 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

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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 at 3 institutions in 2 countries.

Liangqin ShiLaboratory of Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu Sichuan, China.
Chao HuangLaboratory of Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu Sichuan, China.
Qihui LuoLaboratory of Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu Sichuan, China.
Yu XiaLaboratory of Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu Sichuan, China.
Wentao LiuLaboratory of Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu Sichuan, China.
Wen ZengSichuan Primed Biological Technology Co., Ltd, National Experimental Macaque Reproduce Laboratory, Ya'an, Sichuan, China.
Anchun ChengKey Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an, Sichuan, China.
Riyi ShiDepartment of Basic Medical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA.
Chen ZhengliLaboratory of Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu Sichuan, China.
Sichuan Agricultural University · CNPublic Risk Management Association · USPurdue University West Lafayette · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite decades of research into the pathology mechanisms of Parkinson's disease (PD), disease-modifying therapy of PD is scarce. Thus, searching for new drugs or more effective neurosurgical treatments has elicited much interest. Clioquinol (CQ) has been shown to have therapeutic benefits in rodent models of neurodegenerative disorders. However, it's neuroprotective role and mechanisms in PD primate models and PD patients, especially in the advanced stages, are not fully understood. Furthermore, issues such as spontaneous recovery of motor function and high symptom variability in different monkeys after the same toxic protocol, has not been resolved before the present study. In this study, we designed a chronic and long-term progressive protocol to generate a stabilized PD monkey model showed with classic motor and non-motor deficits, followed by treatment analysis of CQ. We found that CQ could remarkably improve the motor and non-motor deficits, which were based on the reduction of iron content and ROS level in the SN and further improvement in pathology. Meanwhile, we also showed that ferroptosis was probably involved in the pathogenesis of PD. In addition, the study shows a positive effect of CQ on AKT/mTOR survival pathway and a blocking effect on p53 medicated cell death

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsClioquinolDisease Models, AnimalHaplorhiniMotor ActivityParkinson DiseaseProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine Kinases1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineClioquinolProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesclioquinolferroptosisironmonkeyParkinson’s disease

Identifiers

PMID32424108
PMCPMC7288933
OpenAlexW3027947998

What OpenQuestion holds

Textmetadata
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.