Brain iron deposition and the free radical-mitochondrial theory of ageing.
Identifieur interne : 002B95 ( Main/Exploration ); précédent : 002B94; suivant : 002B96Brain iron deposition and the free radical-mitochondrial theory of ageing.
Auteurs : Hyman M. Schipper [Canada]Source :
- Ageing research reviews [ 1568-1637 ] ; 2004.
English descriptors
- KwdEn :
- Aging, Alzheimer Disease (etiology), Alzheimer Disease (metabolism), Alzheimer Disease (physiopathology), Animals, Astrocytes (drug effects), Astrocytes (metabolism), Brain (drug effects), Brain (metabolism), Brain (pathology), Catechols (metabolism), Catechols (pharmacology), Central Nervous System Diseases (metabolism), Central Nervous System Diseases (physiopathology), Cysteamine (pharmacology), Free Radicals (metabolism), Gene Expression (drug effects), Heme Oxygenase (Decyclizing) (genetics), Heme Oxygenase (Decyclizing) (metabolism), Heme Oxygenase-1, Humans, Iron (metabolism), Membrane Proteins, Mitochondria (drug effects), Mitochondria (metabolism), Mitochondria (pathology), Models, Biological, Oxidative Stress (physiology), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Peroxidase (metabolism), Superoxide Dismutase (genetics), Superoxide Dismutase (metabolism).
- MESH :
- chemical , genetics : Heme Oxygenase (Decyclizing), Superoxide Dismutase.
- chemical , metabolism : Catechols, Free Radicals, Heme Oxygenase (Decyclizing), Iron, Peroxidase, Superoxide Dismutase.
- drug effects : Astrocytes, Brain, Gene Expression, Mitochondria.
- etiology : Alzheimer Disease.
- metabolism : Alzheimer Disease, Astrocytes, Brain, Central Nervous System Diseases, Mitochondria, Parkinson Disease.
- pathology : Brain, Mitochondria.
- chemical , pharmacology : Catechols, Cysteamine.
- physiology : Oxidative Stress.
- physiopathology : Alzheimer Disease, Central Nervous System Diseases, Parkinson Disease.
- Aging, Animals, Heme Oxygenase-1, Humans, Membrane Proteins, Models, Biological.
Abstract
The central hypothesis of this paper states that oxidative stress, augmented iron deposition, and mitochondrial insufficiency in the ageing and degenerating CNS constitute a single neuropathological 'lesion', and that the advent of one component of this triad obligates the appearance of the others. Evidence in support of this unifying perspective is adduced from human neuropathological studies, experimental paradigms of ageing-associated neurological disorders, and a comprehensive model of astroglial senescence. A pivotal role for the enzyme, heme oxygenase-1 (HO-1) in consolidating this tripartite lesion in the ageing and diseased CNS is emphasized. The data are discussed in the context of a revised 'free radical-mitochondrial-metal' theory of brain ageing, and some scientific and clinical implications of the latter are considered.
DOI: 10.1016/j.arr.2004.02.001
PubMed: 15231237
Affiliations:
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Le document en format XML
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Evidence in support of this unifying perspective is adduced from human neuropathological studies, experimental paradigms of ageing-associated neurological disorders, and a comprehensive model of astroglial senescence. A pivotal role for the enzyme, heme oxygenase-1 (HO-1) in consolidating this tripartite lesion in the ageing and diseased CNS is emphasized. The data are discussed in the context of a revised 'free radical-mitochondrial-metal' theory of brain ageing, and some scientific and clinical implications of the latter are considered.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><country name="Canada"><region name="Québec"><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M" last="Schipper">Hyman M. 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