LRRK2 as a Potential Genetic Modifier of Synucleinopathies: Interlacing the Two Major Genetic Factors of Parkinson's Disease
Experimental Neurobiology
;
: 249-257, 2013.
Artigo
em Inglês
| WPRIM
| ID: wpr-84011
ABSTRACT
Parkinson's disease (PD) and related Lewy body diseases are characterized by deposition of alpha-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 alpha-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 alpha-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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Doença de Parkinson
/
Encéfalo
/
Sistema Nervoso Central
/
Corpos de Lewy
/
Sistema Nervoso Periférico
/
Alfa-Sinucleína
Idioma:
Inglês
Revista:
Experimental Neurobiology
Ano de publicação:
2013
Tipo de documento:
Artigo
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