Evidence for mitochondrial dysfunction in Parkinson's disease--a critical appraisal.
Identifieur interne : 004904 ( Ncbi/Curation ); précédent : 004903; suivant : 004905Evidence for mitochondrial dysfunction in Parkinson's disease--a critical appraisal.
Auteurs : A H Schapira [Royaume-Uni]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1994.
English descriptors
- KwdEn :
- Animals, Blood Platelets (pathology), Blood Platelets (physiology), Brain (pathology), Brain (physiopathology), DNA, Mitochondrial (biosynthesis), Electron Transport (physiology), Humans, Mitochondria (pathology), Mitochondria (physiology), Mitochondria, Muscle (pathology), Mitochondria, Muscle (physiology), Mitochondrial Encephalomyopathies (pathology), Mitochondrial Encephalomyopathies (physiopathology), NAD(P)H Dehydrogenase (Quinone) (deficiency), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Substantia Nigra (pathology), Substantia Nigra (physiopathology).
- MESH :
- chemical , biosynthesis : DNA, Mitochondrial.
- chemical , deficiency : NAD(P)H Dehydrogenase (Quinone).
- pathology : Blood Platelets, Brain, Mitochondria, Mitochondria, Muscle, Mitochondrial Encephalomyopathies, Parkinson Disease, Substantia Nigra.
- physiology : Blood Platelets, Electron Transport, Mitochondria, Mitochondria, Muscle.
- physiopathology : Brain, Mitochondrial Encephalomyopathies, Parkinson Disease, Substantia Nigra.
- Animals, Humans.
Abstract
There is now considerable evidence to support a defect of the mitochondrial respiratory chain, and complex I in particular, in Parkinson's Disease (PD). However, the site specificity of the defect within the chain, its anatomical selectivity within the brain, and its presence in other tissues still remain controversial. Much of the present confusion surrounding the mitochondrial defect can be dispelled by careful analysis of the available data. The molecular basis of the deficiency and its relevance to the pathogenesis of PD remain unknown. Nevertheless, the complex I deficiency in PD provides a direct biochemical link between the idiopathic disease and the MPTP toxin model. The relationship between the mitochondrial defect and other abnormalities within the PD substantia nigra suggests that a self amplifying cycle of events might be precipitated either by a genetic or environmentally induced abnormality of mitochondrial function or free radical metabolism. Alternatively, a biochemical event separate from these might precipitate a cascade which terminates in complex I dysfunction and free radical formation. An understanding of the molecular basis of the complex I defect in PD and its relationship to other biochemical changes will provide important insight into the potential chain of events that lead to dopaminergic cell death in PD.
DOI: 10.1002/mds.870090202
PubMed: 8196673
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Evidence for mitochondrial dysfunction in Parkinson's disease--a critical appraisal.</title><author><name sortKey="Schapira, A H" sort="Schapira, A H" uniqKey="Schapira A" first="A H" last="Schapira">A H Schapira</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurosciences, Royal Free Hospital School of Medicine, London, U.K.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Neurosciences, Royal Free Hospital School of Medicine, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:8196673</idno><idno type="pmid">8196673</idno><idno type="doi">10.1002/mds.870090202</idno><idno type="wicri:Area/PubMed/Corpus">004B42</idno><idno type="wicri:Area/PubMed/Curation">004B42</idno><idno type="wicri:Area/PubMed/Checkpoint">004B29</idno><idno type="wicri:Area/Ncbi/Merge">004904</idno><idno type="wicri:Area/Ncbi/Curation">004904</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Evidence for mitochondrial dysfunction in Parkinson's disease--a critical appraisal.</title><author><name sortKey="Schapira, A H" sort="Schapira, A H" uniqKey="Schapira A" first="A H" last="Schapira">A H Schapira</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurosciences, Royal Free Hospital School of Medicine, London, U.K.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Neurosciences, Royal Free Hospital School of Medicine, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</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="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Blood Platelets (pathology)</term><term>Blood Platelets (physiology)</term><term>Brain (pathology)</term><term>Brain (physiopathology)</term><term>DNA, Mitochondrial (biosynthesis)</term><term>Electron Transport (physiology)</term><term>Humans</term><term>Mitochondria (pathology)</term><term>Mitochondria (physiology)</term><term>Mitochondria, Muscle (pathology)</term><term>Mitochondria, Muscle (physiology)</term><term>Mitochondrial Encephalomyopathies (pathology)</term><term>Mitochondrial Encephalomyopathies (physiopathology)</term><term>NAD(P)H Dehydrogenase (Quinone) (deficiency)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Substantia Nigra (pathology)</term><term>Substantia Nigra (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>DNA, Mitochondrial</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>NAD(P)H Dehydrogenase (Quinone)</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Blood Platelets</term><term>Brain</term><term>Mitochondria</term><term>Mitochondria, Muscle</term><term>Mitochondrial Encephalomyopathies</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Blood Platelets</term><term>Electron Transport</term><term>Mitochondria</term><term>Mitochondria, Muscle</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Mitochondrial Encephalomyopathies</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is now considerable evidence to support a defect of the mitochondrial respiratory chain, and complex I in particular, in Parkinson's Disease (PD). However, the site specificity of the defect within the chain, its anatomical selectivity within the brain, and its presence in other tissues still remain controversial. Much of the present confusion surrounding the mitochondrial defect can be dispelled by careful analysis of the available data. The molecular basis of the deficiency and its relevance to the pathogenesis of PD remain unknown. Nevertheless, the complex I deficiency in PD provides a direct biochemical link between the idiopathic disease and the MPTP toxin model. The relationship between the mitochondrial defect and other abnormalities within the PD substantia nigra suggests that a self amplifying cycle of events might be precipitated either by a genetic or environmentally induced abnormality of mitochondrial function or free radical metabolism. Alternatively, a biochemical event separate from these might precipitate a cascade which terminates in complex I dysfunction and free radical formation. An understanding of the molecular basis of the complex I defect in PD and its relationship to other biochemical changes will provide important insight into the potential chain of events that lead to dopaminergic cell death in PD.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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