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The relevance of iron in the pathogenesis of Parkinson's disease.
MedLine Citation:
PMID:  21138437     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
J. Neurochem. (2011) 118, 939-957. ABSTRACT: Alterations of iron levels in the brain has been observed and documented in a number of neurodegenerative disorders including Parkinson's disease (PD). The elevated nigral iron levels observed in PD may reflect a dysfunction of brain iron homeostasis. Under normal physiological conditions excess iron can be sequestrated in ferritin and neuromelanin. Alternatively, the excess iron may represent a component of brain iron deposition associated with ageing. The aetiology of idiopathic PD largely remains an enigma. However, intensive investigations have provided a host of putative mechanisms that might contribute to the pathogenesis underlying the characteristic degeneration of the dopaminergic neurons in the substantia nigra (SN). The mechanisms proposed include oxidative (and nitrative) stress, inflammation, excitotoxicity, mitochondrial dysfunction, altered proteolysis and finally apoptotic induced cell death. Iron-mediated cellular destruction is mediated primarily via reactive oxygen or/and nitrogen species induced oxidative stress. Furthermore, these pathogenic mechanisms appear to be closely interlinked to the cascade of events leading to cellular death. There are conflicting reports about the stage during disease progression at which nigral iron change occurs in PD. Some have found that there are no changes in iron content SN in asymptomatic incidental Lewy body disease, suggesting it may represent a secondary event in the cascade of neuronal degeneration. In contrast, others have found an elevation of iron in SN in pre-clinical stages. These discrepancies may be attributed to the occurrence of different sub-groups of the disease. This concurs with the notion that PD represents a group of related diseases with a number of potential pathogenic pathways.
Authors:
Jeswinder Sian-Hülsmann; Silvia Mandel; Moussa B H Youdim; Peter Riederer
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Publication Detail:
Type:  Journal Article     Date:  2011-01-31
Journal Detail:
Title:  Journal of neurochemistry     Volume:  118     ISSN:  1471-4159     ISO Abbreviation:  J. Neurochem.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-02     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  939-57     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry.
Affiliation:
Clinical Neurochemistry, National Parkinson Foundation Centre of Excellence Laboratories, Clinic and Polyclinic for Psychiatry, Psychosomatic and Psychotherapy, Medical School, University of Würzburg, Würzburg, Germany Eve Topf Centre of Excellence for Neurodegenerative diseases, Technion-Rappaport Faculty of Medicine, Haifa, Israel Department of Biology, World Central Yonsei University, Seoul, South Korea.
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