Oxidative stress in mitochondria disorders of aging

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Neurons are particularly vulnerable to age-associated decline in mitochondrial function due to their high energy demand. Thus, several models are proposed implicating mtDNA damage and mutation, and subsequent mitochondrial dysfunction, as an underlying factor in a substantial number of human pathologies including aging, neurodegenerative and neuromuscular diseases, and ischemia-reperfusion injury. Furthermore, the results of clinical, biochemical and molecular biology studies suggest that defective mitochondria contribute to neurodegenerative diseases in humans. For example, Friedreich's ataxia exhibits mitochondrial iron overload, Huntington's disease is characterized by defects in mitochondrial oxidative phosphorylation and aconitase deficiency, Parkinson's disease is associated with a deficiency in mitochondrial complex I activity, and Alzheimer's disease exhibits cytochrome oxidase deficiency. Neurologists, psychiatrists and biochemists will profit most from this special issue.