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.