Parkinsons disease is the second common neurodegenerative disorder, after Alzheimers disease. It is a clinical syndrome characterized by loss of dopamine-generating cells in the substancia nigra, a region of the midbrain. The etiology of Parkinsons disease has long been through to involve both genetic and environmental factors. Mutations in the leucine-rich repeat kinase 2 gene cause late-onset Parkinsons disease with a clinical appearance indistinguishable from Parkinsons disease idiopathic. Autophagy is an intracellular catabolic mechanism whereby a cell recycles or degrades damage proteins and cytoplasmic organelles. This degradative process has been associated with cellular dysfunction in neurodegenerative processes including Parkinsons disease. We discuss the role of leucine-rich repeat kinase 2 in autophagy, and how the deregulations of this degradative mechanism in cells can be implicated in the Parkinsons disease etiology. © 2012 José M. Bravo-San Pedro et al.
CITATION STYLE
Bravo-San Pedro, J. M., Gómez-Sánchez, R., Pizarro-Estrella, E., Niso-Santano, M., González-Polo, R. A., & Fuentes Rodríguez, J. M. (2012). Parkinsons disease: Leucine-rich repeat kinase 2 and autophagy, intimate enemies. Parkinson’s Disease. https://doi.org/10.1155/2012/151039
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