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LRRK2 mutant knock-in mouse models: therapeutic relevance in Parkinson's disease
- Source :
- Translational neurodegeneration. 11(1)
- Publication Year :
- 2021
-
Abstract
- 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.
Details
- ISSN :
- 20479158
- Volume :
- 11
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Translational neurodegeneration
- Accession number :
- edsair.doi.dedup.....0b062f3d5b5ec698cb3071cb593f21a8