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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.

LRRK2 mutant knock-in mouse models: therapeutic relevance in Parkinson's disease