Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 20, Issue -, Pages S551-S568Publisher
IOS PRESS
DOI: 10.3233/JAD-2010-100354
Keywords
Alzheimer's disease; FBXL5; iron; iron regulatory protein; iron-sulfur cluster; mitochondria; neurodegeneration; Parkinson's disease
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Funding
- NIH [1P01NS0598 06]
- American Parkinson Disease Association Advanced Center for Parkinson Research at the University of Pittsburgh
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P01NS059806] Funding Source: NIH RePORTER
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In addition to their well-established role in providing the cell with ATP, mitochondria are the source of iron-sulfur clusters (ISCs) and heme - prosthetic groups that are utilized by proteins throughout the cell in various critical processes. The post-transcriptional system that mammalian cells use to regulate intracellular iron homeostasis depends, in part, upon the synthesis of ISCs in mitochondria. Thus, proper mitochondrial function is crucial to cellular iron homeostasis. Many neurodegenerative diseases are marked by mitochondrial impairment, brain iron accumulation, and oxidative stress - pathologies that are interrelated. This review discusses the physiological role that mitochondria play in cellular iron homeostasis and, in so doing, attempts to clarify how mitochondrial dysfunction may initiate and/or contribute to iron dysregulation in the context of neurodegenerative disease. We review what is currently known about the entry of iron into mitochondria, the ways in which iron is utilized therein, and how mitochondria are integrated into the system of iron homeostasis in mammalian cells. Lastly, we turn to recent advances in our understanding of iron dysregulation in two neurodegenerative diseases (Alzheimer's disease and Parkinson's disease), and discuss the use of iron chelation as a potential therapeutic approach to neurodegenerative disease.
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