Evidence map›Paper›PMID 41466978›Full record

ReviewFundamental research2025

Glial cell crosstalk in Parkinson's disease: Mechanisms, implications, and therapeutic strategies.

Ning Wang, Xiao Xiao, Zilu Chen, Keyang Xu, Xiaoyi Cao, Dandan Kou, Jianfeng Zeng

Abstract readReview
In one paragraph

Review in Fundamental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Review
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  6. Article
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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

7 authors.

Ning WangCenter for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School for Radiological and Interdisciplinary Sciences (RAD-X), Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China.
Xiao XiaoCenter for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School for Radiological and Interdisciplinary Sciences (RAD-X), Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China.
Zilu ChenCenter for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School for Radiological and Interdisciplinary Sciences (RAD-X), Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China.
Keyang XuCenter for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School for Radiological and Interdisciplinary Sciences (RAD-X), Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China.
Xiaoyi CaoCenter for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School for Radiological and Interdisciplinary Sciences (RAD-X), Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China.
Dandan KouCenter for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School for Radiological and Interdisciplinary Sciences (RAD-X), Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China.
Jianfeng ZengCenter for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School for Radiological and Interdisciplinary Sciences (RAD-X), Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a prevalent age-related neurodegenerative disorder marked by the progressive loss of dopaminergic neurons and the formation of Lewy bodies. Traditionally viewed as primarily a dopaminergic disorder, recent research has highlighted the significant role of neuroinflammation and the complex interplay between glial cells, particularly astrocytes and microglia, in PD pathogenesis. This review explores the multifaceted roles of astrocytes, microglia and oligodendrocytes in PD, focusing on their involvement in maintaining glutamate and ion homeostasis, energy metabolism, and the inflammatory response. We discuss the dual nature of these glial cells, which can both support and harm neuronal health under different conditions. We also examine the molecular mechanisms underlying glial cell communication, including cytokines, chemokines, extracellular vesicles, gap junctions, and neurotransmitter systems. Finally, we propose potential therapeutic strategies targeting these glial interactions to modulate neuroinflammation and protect neurons, offering new avenues for PD treatment. Understanding the diverse functions and interactions of glial cells in the central nervous system is crucial for developing effective interventions for PD and other neurodegenerative diseases.

Indexed as

Glial CellsMicroglia-astrocyte crosstalkNeurodegenerationNeuroinflammationParkinson's disease

Identifiers

PMID41466978
PMCPMC12744648

What OpenQuestion holds

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LicenceCC BY
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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.