期刊
TRANSLATIONAL NEURODEGENERATION
卷 11, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s40035-022-00285-2
关键词
Parkinson's disease; LRRK2; Knock-in mouse model; Neurotransmission; Motor dysfunction; Autophagy; Lysosome; Mitochondrial dysfunction; Synucleinopathy; Hyperkinase activity; LRRK2 inhibitor
资金
- Tai Hung Fai Charitable Foundation-Edwin S H Leong Research Programme for Parkinson's Disease
- Henry G. Leong Endowed Professorship in Neurology
- Donation Fund for Neurology Research
- Health and Medical Research Fund (HMRF), Food and Health Bureau, Hong Kong S.A.R.
Mutations in the LRRK2 gene are common causes of Parkinson's disease and suggest that LRRK2 could be a therapeutic target. LRRK2 mutant mice models show pathological similarities to early-stage Parkinson's disease, providing important insights into the mechanisms of the disease.
Mutations in the leucine-rich repeat kinase 2 gene (LRRK2) are one of the most frequent genetic causes of both familial and sporadic Parkinson's disease (PD). Mounting evidence has demonstrated pathological similarities between LRRK2-associated PD (LRRK2-PD) and sporadic PD, suggesting that LRRK2 is a potential disease modulator and a therapeutic target in PD. LRRK2 mutant knock-in (KI) mouse models display subtle alterations in pathological aspects that mirror early-stage PD, including increased susceptibility of nigrostriatal neurotransmission, development of motor and non-motor symptoms, mitochondrial and autophagy-lysosomal defects and synucleinopathies. This review provides a rationale for the use of LRRK2 KI mice to investigate the LRRK2-mediated pathogenesis of PD and implications from current findings from different LRRK2 KI mouse models, and ultimately discusses the therapeutic potentials against LRRK2-associated pathologies in PD.
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