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Parkinson’s Disease
Volume 2012, Article ID 429524, 6 pages
Review Article

Parkinson’s Disease and Autophagy

1Clinical and Experimental Neuroscience (NiCE-CIBERNED), School of Medicine, Jaume I University, 12071 Castelló de la Plana, Spain
2Department of Medicine, School of Health Sciences, Jaume I University, Campus Riu Sec, 12071 Castelló de la Plana, Spain
3Department of Neurology, Hospital General Universitari, 12071 Castelló de la Plana, Spain

Received 30 July 2012; Accepted 10 September 2012

Academic Editor: Mireia Niso Santano

Copyright © 2012 Ana María Sánchez-Pérez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It is generally accepted that a correlation between neurodegenerative disease and protein aggregation in the brain exists; however, a causal relationship has not been elucidated. In neurons, failure of autophagy may result in the accumulation of aggregate-prone proteins and subsequent neurodegeneration. Thus, pharmacological induction of autophagy to enhance the clearance of intracytoplasmic aggregate-prone proteins has been considered as a therapeutic strategy to ameliorate pathology in cell and animal models of neurodegenerative disorders. However, autophagy has also been found to be a factor in the onset of these diseases, which raises the question of whether autophagy induction is an effective therapeutic strategy, or, on the contrary, can result in cell death. In this paper, we will first describe the autophagic machinery, and we will consider the literature to discuss the neuroprotective effects of autophagy.