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LRRK2 and membrane trafficking: nexus of Parkinson’s disease
Byoung Dae Lee1,*, Eun-Mi Hur1, Eun-Hae Jang1, Ga Ram Jeong1
1Department of Neuroscience, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul 08826, Republic of Korea,
2Division of Bio-Medical Science &Technology, KIST School, Korea University of Science and Technology, Seoul 02792, South Korea,
3Department of Neuroscience, Kyung Hee University, Seoul 02447, Republic of Korea,
4Department of Physiology, Kyung Hee University School of Medicine, Seoul 02447, Republic of Korea
Abstract
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.
Abstract, Accepted Manuscript [Submitted on July 22, 2019, Accepted on July 22, 2019]
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