Evidence map›Paper›PMID 38566100›Full record

ArticleCell communication and signaling : CCS2024

Single cell analysis reveals the roles and regulatory mechanisms of type-I interferons in Parkinson's disease.

Pusheng Quan, Xueying Li, Yao Si, Linlin Sun, Fei Fan Ding, Yuwei Fan, Han Liu, Chengqun Wei, Ruihua Li, Xue Zhao and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Progenitor CD8Apoptosis : an international journal on programmed cell death · 2026
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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

12 authors at 3 institutions in 1 country.

Pusheng Quan *Department of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Xueying Li *Department of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Yao Si *Department of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Linlin SunDepartment of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Fei Fan DingDepartment of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Yuwei FanDepartment of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Han LiuDepartment of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Chengqun WeiDepartment of General Practice, Heilongjiang Provincial Hospital, Harbin, China.
Ruihua LiDepartment of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Xue ZhaoDepartment of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Fan Yang *Department of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China. yangfan42001@163.com.
Lifen Yao *Department of Neurology, The First Affiliated Hospital, Harbin Medical University, Harbin, China. yaolf@hrbmu.edu.cn.
Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CNHeilongjiang Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of Parkinson's disease (PD) is strongly associated with neuroinflammation, and type I interferons (IFN-I) play a crucial role in regulating immune and inflammatory responses. However, the specific features of IFN in different cell types and the underlying mechanisms of PD have yet to be fully described. In this study, we analyzed the GSE157783 dataset, which includes 39,024 single-cell RNA sequencing results for five PD patients and six healthy controls from the Gene Expression Omnibus database. After cell type annotation, we intersected differentially expressed genes in each cell subcluster with genes collected in The Interferome database to generate an IFN-I-stimulated gene set (ISGs). Based on this gene set, we used the R package AUCell to score each cell, representing the IFN-I activity. Additionally, we performed monocle trajectory analysis, and single-cell regulatory network inference and clustering (SCENIC) to uncover the underlying mechanisms. In silico gene perturbation and subsequent experiments confirm NFATc2 regulation of type I interferon response and neuroinflammation. Our analysis revealed that microglia, endothelial cells, and pericytes exhibited the highest activity of IFN-I. Furthermore, single-cell trajectory detection demonstrated that microglia in the midbrain of PD patients were in a pro-inflammatory activation state, which was validated in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model as well. We identified transcription factors NFATc2, which was significantly up-regulated and involved in the expression of ISGs and activation of microglia in PD. In the 1-Methyl-4-phenylpyridinium (MPP

Indexed as

Interferon Type INeuroblastomaParkinson DiseaseAnimalsEndothelial CellsHumansMiceMice, Inbred C57BLNeuroinflammatory DiseasesNF-kappa BSingle-Cell AnalysisInterferon Type INF-kappa BImmuneParkinson’s diseaseSingle cellTranscription factorsType-I interferons

Identifiers

PMID38566100
PMCPMC10985960
OpenAlexW4393397958

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.