| Apoptosis in Parkinson's disease: Is p53 the missing link between genetic and sporadic Parkinsonism? | |
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MedLine Citation:
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PMID: 20969953 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Parkinson's disease (PD) is a major age-related neurodegenerative disorder characterized by a massive and specific loss of dopaminergic neurons of the substantia nigra pars compacta. The cellular alterations are clinically translated into an invalidating movement disability associated to three canonical symptoms that are bradykinesia, resting tremor and rigidity. The exact causes of this neuronal loss are unknown, but a network of evidences indicates a major contribution of orchestrated cell death processes, also known as apoptosis. Apoptotic cell death is a normal process, the alteration of which triggers several pathologies including cancer and neurodegenerative disorders. Exhaustive work has been done to delineate the cellular mechanisms responsible for the exacerbated cell death of dopaminergic neurons observed in PD. Overall, the oncogene p53 has been identified as a key effector protein. This review will focus on the clues linking p53 to the etiology of PD and the evidences that this protein may be at the center of multiple signaling cascades not only altered by mutations of various proteins responsible for familial cases of PD but also on more general sporadic cases of this devastating disease. |
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Authors:
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Cristine Alves da Costa; Frédéric Checler |
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Publication Detail:
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Type: Journal Article Date: 2010-10-20 |
Journal Detail:
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Title: Cellular signalling Volume: 23 ISSN: 1873-3913 ISO Abbreviation: Cell. Signal. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-03-22 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8904683 Medline TA: Cell Signal Country: England |
Other Details:
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Languages: eng Pagination: 963-8 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Inc. All rights reserved. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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