Gene-modified animal models of Parkinson's disease

被引：0

作者：

Peng, Yong ^{[1
,2
]}

Jiang, Dai-yi ^{[1
,2
]}

Yao, Shun-yu ^{[1
,2
]}

Zhang, Xiuli ^{[3
]}

Kazuo, Sugimoto ^{[4
,5
]}

Liu, Jia ^{[4
,5
]}

Du, Miao-qiao ^{[1
,2
]}

Lin, Lan-xin ^{[1
,2
]}

Chen, Quan ^{[1
,2
]}

Jin, Hong ^{[1
,2
]}

机构：

[1] Hunan Tradit Chinese Med Coll, Affiliated Hosp 1, Dept Neurol, Renmin Rd 571, Zhuzhou 412000, Hunan, Peoples R China

[2] Hunan Univ Chinese Med, Affiliated Prov Tradit Chinese Med Hosp, Dept Neurol, Zhuzhou 412000, Hunan, Peoples R China

[3] Hunan Univ Chinese Med, Sci & Technol Innovat Ctr, Changsha, Peoples R China

[4] Beijing Univ Chinese Med, Dongzhimen Hosp, Dept Neurol, Beijing, Peoples R China

[5] Beijing Univ Chinese Med, Inst Brain Disorders, Beijing, Peoples R China

来源：

EXPERIMENTAL NEUROLOGY | 2025年 / 390卷

关键词：

Parkinson's disease; Gene editing; & Acy; -Synuclein; Autophagy-lysosome pathway; Ubiquitin-proteasome system; Mitochondrial dysfunction; OXIDATIVE STRESS; MOUSE MODEL; MOTOR DEFICITS; S18Y VARIANT; DYSFUNCTION; MICE; MUTATION; NEURONS; NEURODEGENERATION; ATP13A2;

D O I：

10.1016/j.expneurol.2025.115287

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Parkinson's disease (PD) is a neurodegenerative disorder that commonly occurs in older individuals and clinically manifests as resting tremors, bradykinesia, muscle stiffness, and impaired postural balance. From a genetic perspective, animal models using gene-editing technologies offer distinct advantages in replicating the pathophysiological traits of PD, while also functionally exploring potential treatment targets. In this review, we highlight the available gene-modified animal models related to various mechanisms of PD, including abnormal expression of alpha-synuclein protein, dysfunction of the autophagy-lysosome system, abnormalities in the ubiquitin-proteasome system, and mitochondrial dysfunction. We further discuss their respective strengths, limitations, and prospects, aiming to provide the most up to date information for the application of PD animal models and the advancement of anti-PD drugs.

引用

页数：12

共 171 条

[71] α-Synuclein-Independent Histopathological and Motor Deficits in Mice Lacking the Endolysosomal Parkinsonism Protein Atp13a2 [J].