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Review Article

Exp Neurobiol 2013; 22(4): 249-257

Published online December 30, 2013

© The Korean Society for Brain and Neural Sciences

LRRK2 as a Potential Genetic Modifier of Synucleinopathies: Interlacing the Two Major Genetic Factors of Parkinson’s Disease

Cheol Hwan Hyun2#, Chae Young Yoon2#, He-Jin Lee2,3 and Seung-Jae Lee1,2*

1Department of Biomedical Science and Technology, 2Institute of Biomedical Science and Technology, 3Department of Anatomy, School of Medicine, Konkuk University, Seoul 143-701, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-450-4166, FAX: 82-2-447-5683
#These authors contributed equally to this work (alphabetical order).

Received: December 1, 2013; Revised: December 13, 2013; Accepted: December 13, 2013


Parkinson's disease (PD) and related Lewy body diseases are characterized by deposition of α-synuclein aggregates in both the central nervous system and peripheral nervous system. Synucleinopathy lesions spread to larger brain areas as the disease progresses, and prion-like cell-to-cell transmission of aggregated α-synuclein is thought to be the underlying mechanism for this pathological spreading. LRRK2 is another protein linked to the pathogenesis of PD, and its presence in Lewy bodies has attracted much attention as to whether LRRK2 and α-synuclein interplay during the pathogenesis of PD. However, the relationship between these two crucial proteins still remains unclear. In this review article, we will discuss the current state of knowledge in terms of how these proteins cause the disease and provide the hypothetical mechanisms by which LRRK2 might modify the generation and progression of synucleinopathy.

Keywords: Parkinson’s disease, LRRK2, alpha-synuclein, synucleinopathy, transmission, neurodegeneration