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Parkinson's Disease and Autophagy

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 neurodegenerat...

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Autores principales: Sánchez-Pérez, Ana María, Claramonte-Clausell, Berta, Sánchez-Andrés, Juan Vicente, Herrero, María Trinidad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483737/
https://www.ncbi.nlm.nih.gov/pubmed/23125941
http://dx.doi.org/10.1155/2012/429524
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author Sánchez-Pérez, Ana María
Claramonte-Clausell, Berta
Sánchez-Andrés, Juan Vicente
Herrero, María Trinidad
author_facet Sánchez-Pérez, Ana María
Claramonte-Clausell, Berta
Sánchez-Andrés, Juan Vicente
Herrero, María Trinidad
author_sort Sánchez-Pérez, Ana María
collection PubMed
description 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.
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spelling pubmed-34837372012-11-02 Parkinson's Disease and Autophagy Sánchez-Pérez, Ana María Claramonte-Clausell, Berta Sánchez-Andrés, Juan Vicente Herrero, María Trinidad Parkinsons Dis Review Article 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. Hindawi Publishing Corporation 2012 2012-10-17 /pmc/articles/PMC3483737/ /pubmed/23125941 http://dx.doi.org/10.1155/2012/429524 Text en Copyright © 2012 Ana María Sánchez-Pérez et al. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Review Article
Sánchez-Pérez, Ana María
Claramonte-Clausell, Berta
Sánchez-Andrés, Juan Vicente
Herrero, María Trinidad
Parkinson's Disease and Autophagy
title Parkinson's Disease and Autophagy
title_full Parkinson's Disease and Autophagy
title_fullStr Parkinson's Disease and Autophagy
title_full_unstemmed Parkinson's Disease and Autophagy
title_short Parkinson's Disease and Autophagy
title_sort parkinson's disease and autophagy
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483737/
https://www.ncbi.nlm.nih.gov/pubmed/23125941
http://dx.doi.org/10.1155/2012/429524
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