Evidence map›Paper›PMID 36637746›Full record

ArticleMolecular neurobiology2023

Interaction Between the Glymphatic System and α-Synuclein in Parkinson's Disease.

Yu Zhang, Cui Zhang, Xu-Zhong He, Zhen-Hua Li, Jing-Cai Meng, Rui-Ting Mao, Xin Li, Rong Xue, Qian Gui, Guo-Xing Zhang and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 4 pooled it
17.0field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 4 syntheses or guidelines pooled it, 114 citations in OpenAlex.

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19 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Yu Zhang *Department of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Cui Zhang *Department of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Xu-Zhong HeDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Zhen-Hua LiDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Jing-Cai MengDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Rui-Ting MaoDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Xin LiDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Rong XueDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Qian GuiDepartment of Neurology, Suzhou Municipal Hospital, 26 Dao-Qian Street, Suzhou, 215002, People's Republic of China.
Guo-Xing ZhangDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China.
Lin-Hui WangDepartment of Physiology and Neurobiology, Suzhou Medical College of Soochow University, 199 Ren-Ai Road, Suzhou, 215123, People's Republic of China. wanglinhui@suda.edu.cn.ORCID http://orcid.org/0000-0001-5295-324X
Soochow University · CNSuzhou Municipal Hospital · CN

Funding

National Natural Science Foundation of China 31871167
6 · The paper itself

Abstract

The glymphatic system contributes to the clearance of amyloid-β from the brain and is disrupted in Alzheimer's disease. However, whether the system is involved in the removal of α-synuclein (α-syn) and whether it is suppressed in Parkinson's disease (PD) remain largely unknown. In mice receiving the intranigral injection of recombinant human α-syn, we found that the glymphatic suppression via aquaporin-4 (AQP4) gene deletion or acetazolamide treatment reduced the clearance of injected α-syn from the brain. In mice overexpressing the human A53T-α-syn, we revealed that AQP4 deficiency accelerated the accumulation of α-syn, facilitated the loss of dopaminergic neurons, and accelerated PD-like symptoms. We also found that the overexpression of A53T-α-syn reduced the expression/polarization of AQP4 and suppressed the glymphatic activity of mice. The study demonstrates a close interaction between the AQP4-mediated glymphatic system and parenchymal α-syn, indicating that restoring the glymphatic activity is a potential therapeutic target to delay PD progression.

Indexed as

Alzheimer DiseaseGlymphatic SystemParkinson Diseasealpha-SynucleinAnimalsBrainHumansMicealpha-SynucleinAquaporin-4Cerebrospinal fluidGlymphatic systemParkinson’s diseaseα-Synuclein

Identifiers

PMID36637746
OpenAlexW4315928004

What OpenQuestion holds

Textmetadata
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.