Author:
Chang Eunice Eun Seo,Ho Philip Wing-Lok,Liu Hui-Fang,Pang Shirley Yin-Yu,Leung Chi-Ting,Malki Yasine,Choi Zoe Yuen-Kiu,Ramsden David Boyer,Ho Shu-Leong
Abstract
AbstractMutations 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.
Funder
Tai Hung Fai Charitable Foundation - Edwin S H Leong Research Programme for Parkinson’s Disease
The Henry G. Leong Endowed Professorship in Neurology
The Donation Fund for Neurology Research
Health and Medical Research Fund
Publisher
Springer Science and Business Media LLC
Subject
Cellular and Molecular Neuroscience,Cognitive Neuroscience,Neurology (clinical)
Cited by
13 articles.
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