Research progress on animal models of Parkinson disease
10.3969/j.issn.1002-0152.2025.03.011
- VernacularTitle:帕金森病动物模型研究进展
- Author:
Ziyu WANG
1
;
Xiaohui WANG
1
Author Information
1. 上海体育大学运动健康学院(上海 200438)
- Publication Type:Journal Article
- Keywords:
Parkinson disease;
Animal model;
Ubiquitin protease system;
Autophagy lysosomal system;
Genetic engineering
- From:
Chinese Journal of Nervous and Mental Diseases
2025;51(3):186-192
- CountryChina
- Language:Chinese
-
Abstract:
Parkinson disease(PD)is defined by two hallmark pathological features:the progressive degeneration of dopaminergic(DAergic)neurons in the substantia nigra pars compacta(SNc)and the pathological aggregation of alpha-synuclein(α-syn).Despite extensive research,the molecular mechanisms driving PD remain incompletely understood,and effective treatments are still lacking.Growing evidence implicates α-syn aggregation and impaired protein clearance—particularly through dysfunction of the autophagy-lysosomal pathway(ALP)and ubiquitin-proteasome system(UPS)—as central contributors to neurodegeneration through disrupted proteostasis.Genetically engineered rodent models,developed using advanced gene-editing tools,faithfully replicate core PD pathological features,including α-syn aggregation dynamics,selective neuronal vulnerability,and motor deficits.These models serve as indispensable platforms for dissecting α-syn-mediated toxicity mechanisms.By identifying critical regulatory nodes in α-syn homeostasis,they provide a strategic foundation for therapies targeting clearance pathway restoration or aggregation inhibition,positioning themselves as essential tools for overcoming current therapeutic limitations in PD.
