期刊
BMB REPORTS
卷 52, 期 9, 页码 533-539出版社
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2019.52.9.186
关键词
LRRK2; Parkinson's disease; Rab; Synaptic vesicle; Vesicle trafficking
资金
- Research Resettlement Fund for the new faculty of Seoul National University [55020180037]
- Research Institute for Veterinary Science, Seoul National University
- Brain Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science, ICT & Future Planning [NRF-2016M3C7A1905386, 2017M3C7A1043848]
- National Research Foundation of Korea [2017M3C7A1043848, 2016M3C7A1905386] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Recent evidence from genetics, animal model systems and biochemical studies suggests that defects in membrane trafficking play an important part in the pathophysiology of Parkinson's disease (PD). Mutations in leucine-rich repeat kinase 2 (LRRK2) constitute the most frequent genetic cause of both familial and sporadic PD, and LRRK2 has been suggested as a druggable target for PD. Although the precise physiological function of LRRK2 remains largely unknown, mounting evidence suggests that LRRK2 controls membrane trafficking by interacting with key regulators of the endosomal-lysosomal pathway and synaptic recycling. In this review, we discuss the genetic, biochemical and functional links between LRRK2 and membrane trafficking. Understanding the mechanism by which LRRK2 influences such processes may contribute to the development of disease-modifying therapies for PD.
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