Evidence map›Paper›PMID 41653051›Full record

ArticleBrain : a journal of neurology2026

α-Synuclein aggregation and brain atrophy in SNCA-A53T transgenic monkeys are correlated with parkinsonism.

Jingkuan Wei, Shulin Li, Dingna Duan, Kunhua Wu, Xu Liu, Ran Zhu, Li Wang, Zhengwang Wu, Yu Kang, Chenyang Si and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain : a journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Jingkuan WeiState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.ORCID 0000-0001-7528-4034
Shulin LiState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Dingna DuanDepartment of Radiology and BRIC, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Kunhua WuDepartment of MRI, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan 650032, China.
Xu LiuState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Ran ZhuState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Li WangDepartment of Radiology and BRIC, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Zhengwang WuDepartment of Radiology and BRIC, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Yu KangState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Chenyang SiState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Hongjiang ZhangDepartment of MRI, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan 650032, China.
Hong WangState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Yongchang ChenState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Shaoxing DaiState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Weizhi JiState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Gang LiDepartment of Radiology and BRIC, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Lu ZhaoState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.
Yuyu NiuState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, China.ORCID 0000-0002-8797-4152

Funding

Changping Laboratory 2025B-07-17National Key Research and Development Program 2021YFA0805702National Natural Science Foundation of China 32060190National Natural Science Foundation of China 32070541National Natural Science Foundation of China 32260197National Natural Science Foundation of China U2102204Natural Science Foundation of Yunnan 202301AT070476Natural Science Foundation of Yunnan 202401AS070040Natural Science Foundation of Yunnan 202507AB040007
6 · The paper itself

Abstract

Mutations in the SNCA gene encoding α-synuclein underlie familial early-onset Parkinson's disease. Pathological α-synuclein deposition may commence decades prior to the emergence of cardinal motor symptoms. Long-term investigation of brain and behavioural development in an SNCA-A53T transgenic macaque model offers critical insights into Parkinson's disease progression. In this study, we systematically characterized SNCA-A53T transgenic rhesus monkeys through multimodal assessments. Our results showed that these transgenic monkeys exhibited phosphorylated α-synuclein aggregation patterns and dopaminergic degeneration resembling Parkinson's disease patients. Progressive motor and cognitive deficits were observed in transgenic monkeys with ageing. Polysomnographic analysis revealed rapid eye movement sleep behaviour disorder manifestations in transgenic animals. Four-year longitudinal MRI tracking demonstrated abnormal developmental patterns of cortical surface area alongside alterations in thickness and volume. The single-cell transcriptome revealed that astrocyte-specific gene dysregulation and cell loss contribute to brain atrophy in transgenic monkeys. Cortical and subcortical grey matter regions showing volume reduction were functionally associated with behavioural deficits and differentiated transgenic animals from wild-type controls. Collectively, this comprehensive study provides evidence that SNCA-A53T transgenic monkeys recapitulate Parkinson's disease pathophysiology while demonstrating the utility of longitudinal monitoring in genetically engineered non-human primates for tracking neurodegenerative disease progression.

Indexed as

alpha-SynucleinBrainParkinsonian DisordersAnimalsAnimals, Genetically ModifiedAtrophyDisease Models, AnimalFemaleHumansMacaca mulattaMagnetic Resonance ImagingMaleREM Sleep Behavior Disorderalpha-Synucleinbrain structureMRIParkinson’s diseaseREM sleep behaviour disordersleep disturbancetransgenic monkeys

Identifiers

PMID41653051
PMCPMC13548855

What OpenQuestion holds

Textmetadata
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Registered trials

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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.