L‐Dihydroxyphenylalanine and complex I deficiency in Parkinson's disease brain
Identifieur interne : 005874 ( Main/Exploration ); précédent : 005873; suivant : 005875L‐Dihydroxyphenylalanine and complex I deficiency in Parkinson's disease brain
Auteurs : J. M. Cooper [Royaume-Uni] ; S. E. Daniel [Royaume-Uni] ; C. D. Marsden [Royaume-Uni] ; Schapira [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1995-05.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Brain (drug effects), Brain (pathology), Complex I, Female, Humans, Levodopa (adverse effects), L‐Dihydroxyphenylalanine, Male, Middle Aged, NAD(P)H Dehydrogenase (Quinone) (deficiency), Nerve Degeneration (drug effects), Nerve Degeneration (physiology), Neural Pathways (drug effects), Neural Pathways (pathology), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson's disease, Putamen (drug effects), Putamen (pathology), Substantia Nigra (drug effects), Substantia Nigra (pathology).
- MESH :
- chemical , adverse effects : Levodopa.
- chemical , deficiency : NAD(P)H Dehydrogenase (Quinone).
- drug effects : Brain, Nerve Degeneration, Neural Pathways, Putamen, Substantia Nigra.
- drug therapy : Parkinson Disease.
- pathology : Brain, Neural Pathways, Parkinson Disease, Putamen, Substantia Nigra.
- physiology : Nerve Degeneration.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged.
Abstract
There is evidence for a 37% deficiency of complex I activity in Parkinson's disease (PD), which appears to be specific for PD amongst parkinsonian syndromes and selective for the substantia nigra within the central nervous system. Rat studies have shown that, in the context of a normal nigrostriatal dopaminergic cell population, L‐dihydroxyphenylalanine (L‐dopa) causes a reversible 25% defect of complex I activity in nigral and striatal tissue. Analysis of striatal tissue from PD patients after prolonged exposure to highdose L‐dopa does not show such a defect. Results of these and other studies suggest that L‐dopa therapy does not cause complex I deficiency in PD striatum. However, it cannot be excluded that, in the particular environment of the PD substantia nigra, L‐dopa may enhance a preexisting complex I defect.
Url:
DOI: 10.1002/mds.870100311
Affiliations:
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M." last="Cooper">J. M. Cooper</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, Queen Square, London</wicri:cityArea></affiliation></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S. E." last="Daniel">S. E. Daniel</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Institute of Neurology, Queen Square, London</wicri:cityArea></affiliation></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Institute of Neurology, Queen Square, London</wicri:cityArea></affiliation></author><author><name sortKey="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, Queen Square, London</wicri:cityArea></affiliation><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Institute of Neurology, Queen Square, London</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-05">1995-05</date><biblScope unit="vol">10</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="295">295</biblScope><biblScope unit="page" to="297">297</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">B69EB49C8AFE92CE44D8B48EEEC9B78C25F20F1E</idno><idno type="DOI">10.1002/mds.870100311</idno><idno type="ArticleID">MDS870100311</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Brain (drug effects)</term><term>Brain (pathology)</term><term>Complex I</term><term>Female</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>L‐Dihydroxyphenylalanine</term><term>Male</term><term>Middle Aged</term><term>NAD(P)H Dehydrogenase (Quinone) (deficiency)</term><term>Nerve Degeneration (drug effects)</term><term>Nerve Degeneration (physiology)</term><term>Neural Pathways (drug effects)</term><term>Neural Pathways (pathology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (pathology)</term><term>Parkinson's disease</term><term>Putamen (drug effects)</term><term>Putamen (pathology)</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>NAD(P)H Dehydrogenase (Quinone)</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term><term>Nerve Degeneration</term><term>Neural Pathways</term><term>Putamen</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Neural Pathways</term><term>Parkinson Disease</term><term>Putamen</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is evidence for a 37% deficiency of complex I activity in Parkinson's disease (PD), which appears to be specific for PD amongst parkinsonian syndromes and selective for the substantia nigra within the central nervous system. Rat studies have shown that, in the context of a normal nigrostriatal dopaminergic cell population, L‐dihydroxyphenylalanine (L‐dopa) causes a reversible 25% defect of complex I activity in nigral and striatal tissue. Analysis of striatal tissue from PD patients after prolonged exposure to highdose L‐dopa does not show such a defect. Results of these and other studies suggest that L‐dopa therapy does not cause complex I deficiency in PD striatum. However, it cannot be excluded that, in the particular environment of the PD substantia nigra, L‐dopa may enhance a preexisting complex I defect.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Cooper, J M" sort="Cooper, J M" uniqKey="Cooper J" first="J. M." last="Cooper">J. M. Cooper</name></region><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S. E." last="Daniel">S. E. Daniel</name><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><name sortKey="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name><name sortKey="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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