A rationale for monoamine oxidase inhibition as neuroprotective therapy for Parkinson's disease.
Identifieur interne : 008F40 ( Main/Merge ); précédent : 008F39; suivant : 008F41A rationale for monoamine oxidase inhibition as neuroprotective therapy for Parkinson's disease.
Auteurs : C W Olanow [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
- Free Radicals, Humans, Lipid Peroxidation (drug effects), Lipid Peroxidation (physiology), Monoamine Oxidase Inhibitors (therapeutic use), Nerve Degeneration (drug effects), Nerve Degeneration (physiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Reactive Oxygen Species (metabolism), Selegiline (therapeutic use), Substantia Nigra (drug effects), Substantia Nigra (physiopathology).
- MESH :
- chemical , metabolism : Reactive Oxygen Species.
- chemical , therapeutic use : Monoamine Oxidase Inhibitors, Selegiline.
- chemical : Free Radicals.
- drug effects : Lipid Peroxidation, Nerve Degeneration, Substantia Nigra.
- drug therapy : Parkinson Disease.
- physiology : Lipid Peroxidation, Nerve Degeneration.
- physiopathology : Parkinson Disease, Substantia Nigra.
- Humans.
Abstract
Neurons in the substantia nigra may be vulnerable to oxidant stress because (a) the metabolism of dopamine generates peroxides, which, in the presence of iron, can lead to the formation of the highly reactive hydroxyl free radical; and (b) neuromelanin within nigral neurons can bind metals such as iron and aluminum and thereby promote the site-specific formation of free radicals. Postmortem studies show increased iron, decreased glutathione, and increased lipid peroxidation in the substantia nigra of patients with Parkinson's disease (PD). Recent studies also report iron and aluminum accumulation within neuromelanin granules of patients with PD. These findings suggest that the substantia nigra in the patient with PD is in a state of oxidant stress and that antioxidant therapy might protect residual dopamine neurons and slow the natural progression of PD. Selective inhibitors of monoamine oxidase type B (MAO-B) have been chosen for study because of their capacity to interfere with the oxidative metabolism of dopamine and so diminish the likelihood that free radicals will be formed. Initial studies demonstrate that the MAO-B inhibitor L-deprenyl (selegiline) delays the development of disability in otherwise untreated patients with early Parkinson's disease. Although the mechanism responsible for these observations remains unclear, these results are consistent with the possibility that L-deprenyl provides neuroprotective effects.
PubMed: 8302302
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pubmed:8302302Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A rationale for monoamine oxidase inhibition as neuroprotective therapy for Parkinson's disease.</title><author><name sortKey="Olanow, C W" sort="Olanow, C W" uniqKey="Olanow C" first="C W" last="Olanow">C W Olanow</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neurology, Psychiatry and Pharmacology, University of South Florida, Tampa.</nlm:affiliation><orgName type="university">Université de Floride du Sud</orgName><country>États-Unis</country><placeName><settlement type="city">Tampa</settlement><region type="state">Floride</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1993">1993</date><idno type="RBID">pubmed:8302302</idno><idno type="pmid">8302302</idno><idno type="wicri:Area/PubMed/Corpus">004C96</idno><idno type="wicri:Area/PubMed/Curation">004C96</idno><idno type="wicri:Area/PubMed/Checkpoint">004C96</idno><idno type="wicri:Area/Ncbi/Merge">004945</idno><idno type="wicri:Area/Ncbi/Curation">004945</idno><idno type="wicri:Area/Ncbi/Checkpoint">004945</idno><idno type="wicri:doubleKey">0885-3185:1993:Olanow C:a:rationale:for</idno><idno type="wicri:Area/Main/Merge">008F40</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A rationale for monoamine oxidase inhibition as neuroprotective therapy for Parkinson's disease.</title><author><name sortKey="Olanow, C W" sort="Olanow, C W" uniqKey="Olanow C" first="C W" last="Olanow">C W Olanow</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neurology, Psychiatry and Pharmacology, University of South Florida, Tampa.</nlm:affiliation><orgName type="university">Université de Floride du Sud</orgName><country>États-Unis</country><placeName><settlement type="city">Tampa</settlement><region type="state">Floride</region></placeName></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Free Radicals</term><term>Humans</term><term>Lipid Peroxidation (drug effects)</term><term>Lipid Peroxidation (physiology)</term><term>Monoamine Oxidase Inhibitors (therapeutic use)</term><term>Nerve Degeneration (drug effects)</term><term>Nerve Degeneration (physiology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Reactive Oxygen Species (metabolism)</term><term>Selegiline (therapeutic use)</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Monoamine Oxidase Inhibitors</term><term>Selegiline</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Free Radicals</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lipid Peroxidation</term><term>Nerve Degeneration</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lipid Peroxidation</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neurons in the substantia nigra may be vulnerable to oxidant stress because (a) the metabolism of dopamine generates peroxides, which, in the presence of iron, can lead to the formation of the highly reactive hydroxyl free radical; and (b) neuromelanin within nigral neurons can bind metals such as iron and aluminum and thereby promote the site-specific formation of free radicals. Postmortem studies show increased iron, decreased glutathione, and increased lipid peroxidation in the substantia nigra of patients with Parkinson's disease (PD). Recent studies also report iron and aluminum accumulation within neuromelanin granules of patients with PD. These findings suggest that the substantia nigra in the patient with PD is in a state of oxidant stress and that antioxidant therapy might protect residual dopamine neurons and slow the natural progression of PD. Selective inhibitors of monoamine oxidase type B (MAO-B) have been chosen for study because of their capacity to interfere with the oxidative metabolism of dopamine and so diminish the likelihood that free radicals will be formed. Initial studies demonstrate that the MAO-B inhibitor L-deprenyl (selegiline) delays the development of disability in otherwise untreated patients with early Parkinson's disease. Although the mechanism responsible for these observations remains unclear, these results are consistent with the possibility that L-deprenyl provides neuroprotective effects.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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