IIBBA   05544
INSTITUTO DE INVESTIGACIONES BIOQUIMICAS DE BUENOS AIRES
Unidad Ejecutora - UE
artículos
Título:
LRRK-2 as a Key Molecule Bridging Inflammation to Parkinson's Disease
Autor/es:
ROCA; PUNTEL
Revista:
Advances in Neuroimmune Biology
Editorial:
IOS press
Referencias:
Año: 2013 vol. 4 p. 205 - 215
ISSN:
1878-9498
Resumen:
The pathogenetic mechanisms leading to typical Parkinson?s Disease (PD), the second most common human neurodegenerativedisorder remains unknown. Genetic variants of Leucine-Rich Repeat Kinase 2 (LRRK-2) are associated witha significantly enhanced risk for PD. The discovery that late-onset PD could be caused by the inheritance of a mutation inthe LRRK-2 gene leading to familial as well as sporadic forms of PD has provided researchers an opportunity to explore thepathophysiological events underlying this complex disease. Despite extensive research our understanding of LRRK-2 biologicalfunction and regulation remains rudimentary. In this review, we give an insight into the role of LRRK-2 in modulating inflammationin the central nervous system and we hypothesize that LRRK-2 dysfunction may favor the neurodegenerative processobserved in PD.