Mitochondrial iron-sulfur cluster dysfunction in neurodegenerative disease

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Mitochondrial iron-sulfur cluster dysfunction in neurodegenerative disease

Growing evidence supports a role for mitochondrial iron metabolism in the pathophysiology of neurodegenerative disorders such as Friedreich ataxia (FRDA) and Parkinson disease (PD) as well as in the motor and cognitive decline associated with the aging process. Iron-sulfur enzyme deficits and regional iron accumulation have been observed in each of these conditions. In spite of significant etio...

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Iron-sulfur [Fe-S] clusters are prosthetic groups required to maintain life processes including respiration, photosynthesis, metabolic reactions, sensing, signaling,and gene regulation. In plants the biogenesis of Fe-S proteins is compartmentalized and adapted to specific needs of the eukaryotic and photosynthetic cell. Although critical to so many fundamental metabolic pathways and drastically...

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Iron-sulfur cluster biogenesis and human disease.

Iron-sulfur (Fe-S) clusters are essential for numerous biological processes, including mitochondrial respiratory chain activity and various other enzymatic and regulatory functions. Human Fe-S cluster assembly proteins are frequently encoded by single genes, and inherited defects in some of these genes cause disease. Recently, the spectrum of diseases attributable to abnormal Fe-S cluster bioge...

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Mitochondrial Dysfunction Leads to Nuclear Genome Instability via an Iron-Sulfur Cluster Defect

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Mitochondrial dysfunction in neurodegenerative disorders.

There is compelling evidence for the direct involvement of mitochondria in certain neurodegenerative disorders, such as Morbus Parkinson, FRDA (Friedreich's ataxia), ALS (amyotrophic lateral sclerosis), and temporal lobe epilepsy with Ammon's horn sclerosis. This evidence includes the direct genetic evidence of pathogenic mutations in mitochondrial proteins in inherited Parkinsonism {such as PA...

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ژورنال

عنوان ژورنال: Frontiers in Pharmacology

سال: 2014

ISSN: 1663-9812

DOI: 10.3389/fphar.2014.00029