Single-cell atlas of neuroglial dynamics in SNCA-A53T Parkinson's disease mouse model.
Overview
- Hubei Key Laboratory of Wudang Local Chinese Medicine Research, Research Center for Translational Medicine of Xiangyang No. 1 People's Hospital, Hubei Provincial Clinical Research Center for Parkinson's Disease at Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Shiyan, China
- Department of Industrial Engineering, Center for Statistical Science, Tsinghua University, Beijing, China
- Genertec Gem Flower Healthcare, Clinical Laboratory of Gem Flower Xian Changqing Staff Hospital, Xi'an, China
Abstract
Background: Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive degeneration of midbrain substantia nigra dopaminergic neurons, resulting in striatal dopamine depletion and motor dysfunction. While this pathological cascade is well‐established, its underlying mechanisms remain elusive.
Methods: To further investigate the pathological mechanisms of PD, we performed single‐cell RNA sequencing of the midbrain and striatum from Hua‐Syn (SNCA*A53T) transgenic (A53T) mice as a PD model.
Results: Analysis of 22 865 midbrain and 32 117 striatal cells revealed cell‐type‐specific risk association. Glial populations (astrocytes, microglia, oligodendrocytes) showed significant enrichment for PD‐risk genes. Variance‐based clustering identified PD‐enriched subclusters exhibiting upregulated inflammatory pathways, apoptotic pathways, proteostasis disruption, glutamatergic signaling dysregulation, and mitochondrial respiratory chain defects. Transcriptional regulation analysis identified genes associated with PD specific activity, including Rorb and Foxc1 in the midbrain and Dbx2 and Klf13 in the striatum. Cell–cell interactions showed that cell‐to‐cell signaling was enhanced, and the SEMA and CCL neuroinflammatory axes were specifically activated in the PD group.
Conclusions: Our integrative analysis delineates the cellular and molecular architecture of the pathological process triggered by the expression of A53T mutant α‐synuclein, and provides a framework for targeted therapeutic development.
Reproduced under the paper's license (CC BY-NC), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE157783, at NCBI GEO; found in the text, “Regulation of RORB and FOXC1 in the human…”
Other data links
- ncbi.nlm.nih.gov/
geo , NCBI; found in the text, “Regulation of RORB and FOXC1 in the human…”
Data availability statement
The data presented in the study are deposited in the NCBI Sequence Read Archive repository, accession number GSE306642 (https://
Reproduced under the paper's license (CC BY-NC), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 8 authors, 5 keywords, 11 MeSH terms, 5 funders, 44 references.
Cite
This paper
Qin, B., Fu, Z., Zou, X., Chai, S., Weng, J., Wang, P., Sun, X., & Sang, M. (2026). Single-cell atlas of neuroglial dynamics in SNCA-A53T Parkinson's disease mouse model. Animal models and experimental medicine, 9(8), 1613-1632. https://
BibTeX
@article{qin2026single,
author = {Qin, Binqing and Fu, Zichu and Zou, Xuanxuan and Chai, Senmao and Weng, Jingjing and Wang, Puqing and Sun, Xiaodong and Sang, Ming},
title = {{Single-cell atlas of neuroglial dynamics in SNCA-A53T Parkinson's disease mouse model}},
journal = {Animal models and experimental medicine},
year = {2026},
month = jul,
volume = {9},
number = {8},
pages = {1613--1632},
publisher = {Wiley},
issn = {2096-5451},
doi = {10.1002/
url = {https://
pmid = {42447147},
pmcid = {PMC13394255}
}
RIS
TY - JOUR
AU - Qin, Binqing
AU - Fu, Zichu
AU - Zou, Xuanxuan
AU - Chai, Senmao
AU - Weng, Jingjing
AU - Wang, Puqing
AU - Sun, Xiaodong
AU - Sang, Ming
TI - Single-cell atlas of neuroglial dynamics in SNCA-A53T Parkinson's disease mouse model
T2 - Animal models and experimental medicine
J2 - Animal Model Exp Med
PY - 2026
DA - 2026/
VL - 9
IS - 8
SP - 1613
EP - 1632
SN - 2096-5451
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1002/
"type": "article-journal",
"title": "Single-cell atlas of neuroglial dynamics in SNCA-A53T Parkinson's disease mouse model",
"container-title": "Animal models and experimental medicine",
"author": [
{
"family": "Qin",
"given": "Binqing"
},
{
"family": "Fu",
"given": "Zichu"
},
{
"family": "Zou",
"given": "Xuanxuan"
},
{
"family": "Chai",
"given": "Senmao"
},
{
"family": "Weng",
"given": "Jingjing"
},
{
"family": "Wang",
"given": "Puqing"
},
{
"family": "Sun",
"given": "Xiaodong"
},
{
"family": "Sang",
"given": "Ming"
}
],
"container-title-short":
"volume": "9",
"issue": "8",
"page": "1613-1632",
"DOI": "10.1002/
"PMID": "42447147",
"PMCID": "PMC13394255",
"ISSN": "2096-5451",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
7,
14
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1101/gr.281113.125 [code]
- Single-nucleus multiomic profiling of the aging mouse substantia nigra reveals conserved gene alterations linked to Parkinson's disease.Journal: Genome researchIn common: Parkinson's, genetics / omics, mouse, 1 other category, 6 references
- [2] doi:10.1002/advs.77175
- TAB2 Causes Neuronal Damage by Aggravating Microglia-Mediated Neuroinflammation in Parkinson's Disease.Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)In common: NCBI GEO GSE157783, Parkinson's, cellular / molecular, 2 references
- [3] doi:10.1186/s13195-026-02081-w [code]
- Cellular state heterogeneity underlying sex differences in Alzheimer's disease based on single-cell transcriptome.Journal: Alzheimer's research & therapyIn common: genetics / omics, cellular / molecular, 4 references
- [4] doi:10.3390/ijms27167140
- Astrocytic HSP90AA1 Upregulation and Altered Synaptic Signaling in Parkinson's Disease: Transcriptomic Screening and In Vivo Validation.Journal: International journal of molecular sciencesIn common: Parkinson's, genetics / omics, mouse, 1 other category, 3 references
- [5] doi:10.3389/fnins.2026.1862571
- Integrated bulk, single-cell, and spatial transcriptomic analyses prioritize NOTCH1 as a candidate gene associated with neurovascular and immune-related alterations in Parkinson's disease.Journal: Frontiers in neuroscienceIn common: Parkinson's, genetics / omics, mouse, 1 other category, 3 references
- [6] doi:10.1038/s41597-026-07185-4 [code]
- A multi-center cross-platform single-cell multimodal atlas of the mouse cerebral cortex.Journal: Scientific dataIn common: genetics / omics, mouse, 4 references
- [7] doi:10.1038/s41588-026-02709-5
- PLCG2 downregulation impairs synaptic function and increases Alzheimer's disease hallmarks in neuronal cultures.Journal: Nature geneticsIn common: genetics / omics, mouse, cellular / molecular, 3 references
- [8] doi:10.1186/s12967-026-08706-w
- Impaired NADH-linked mitochondrial respiration disrupts ventral midbrain neuronal programs in POLG disease.Journal: Journal of translational medicineIn common: genetics / omics, cellular / molecular, 3 references
- [9] doi:10.1038/s41586-026-10679-1 [code]
- Cortical development dynamics across autism spectrum disorder mouse models.Journal: NatureIn common: genetics / omics, mouse, cellular / molecular, 3 references
- [10] doi:10.1126/sciadv.aed6825
- SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain.Journal: Science advancesIn common: genetics / omics, mouse, cellular / molecular, 3 references
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.