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Oxidative Medicine and Cellular Longevity
Volume 2012 (2012), Article ID 128647, 8 pages
Review Article

Iron and Neurodegeneration: From Cellular Homeostasis to Disease

Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, EAN, Avenida da República, 2781-901 Oeiras, Portugal

Received 10 February 2012; Revised 21 March 2012; Accepted 5 April 2012

Academic Editor: Marcos Dias Pereira

Copyright © 2012 Liliana Batista-Nascimento 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.


Accumulation of iron (Fe) is often detected in the brains of people suffering from neurodegenerative diseases. High Fe concentrations have been consistently observed in Parkinson’s, Alzheimer’s, and Huntington’s diseases; however, it is not clear whether this Fe contributes to the progression of these diseases. Other conditions, such as Friedreich’s ataxia or neuroferritinopathy are associated with genetic factors that cause Fe misregulation. Consequently, excessive intracellular Fe increases oxidative stress, which leads to neuronal dysfunction and death. The characterization of the mechanisms involved in the misregulation of Fe in the brain is crucial to understand the pathology of the neurodegenerative disorders and develop new therapeutic strategies. Saccharomyces cerevisiae, as the best understood eukaryotic organism, has already begun to play a role in the neurological disorders; thus it could perhaps become a valuable tool also to study the metalloneurobiology.