Mitochondrial DNA analysis in Parkinson's disease
Identifieur interne : 006300 ( Main/Exploration ); précédent : 006299; suivant : 006301Mitochondrial DNA analysis in Parkinson's disease
Auteurs : Schapira [Royaume-Uni] ; I. J. Holt [Royaume-Uni] ; M. Sweeney [Royaume-Uni] ; A. E. Harding [Royaume-Uni] ; P. Jenner [Royaume-Uni] ; C. D. Marsden [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1990.
Descripteurs français
- Wicri :
- topic : ADN.
English descriptors
- KwdEn :
- Complex I, DNA, DNA Damage (genetics), DNA, Mitochondrial (analysis), Humans, Mitochondria, NAD(P)H Dehydrogenase (Quinone), Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson's disease, Polymorphism, Restriction Fragment Length, Quinone Reductases (deficiency), Substantia Nigra (pathology).
- MESH :
- chemical , analysis : DNA, Mitochondrial.
- chemical , deficiency : Quinone Reductases.
- genetics : DNA Damage, Parkinson Disease.
- pathology : Parkinson Disease, Substantia Nigra.
- Humans, NAD(P)H Dehydrogenase (Quinone), Polymorphism, Restriction Fragment Length.
Abstract
The reduced form of nicotinamide adenine dinucleotide coenzyme Q reductase (complex I) activity has recently been shown to be deficient in the substantia nigra of patients dying with Parkinson's disease. This biochemical defect is identical to that produced by the neurotoxin 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP), which also produces parkinsonism in humans. Complex I comprises 25 polypeptides, seven of which are encoded by mitochondrial DNA. Restriction fragment analysis of substantia nigra DNA from six patients with Parkinson's disease did not show any major deletion. In two cases, there were different novel polymorphisms that were not observed in control brain (n = 6) or blood (n = 34) samples.
Url:
DOI: 10.1002/mds.870050406
Affiliations:
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Marsden</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology, Institute of Neurology, Pharmacology Group, Biomedical Science Division, King's College Hospital, 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="1990">1990</date><biblScope unit="vol">5</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="294">294</biblScope><biblScope unit="page" to="297">297</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">F2810D4495BF4CAC16D0920A6F250B5E16B33DB0</idno><idno type="DOI">10.1002/mds.870050406</idno><idno type="ArticleID">MDS870050406</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Complex I</term><term>DNA</term><term>DNA Damage (genetics)</term><term>DNA, Mitochondrial (analysis)</term><term>Humans</term><term>Mitochondria</term><term>NAD(P)H Dehydrogenase (Quinone)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson's disease</term><term>Polymorphism, Restriction Fragment Length</term><term>Quinone Reductases (deficiency)</term><term>Substantia Nigra (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>DNA, Mitochondrial</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Quinone Reductases</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>ADN</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>DNA Damage</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>NAD(P)H Dehydrogenase (Quinone)</term><term>Polymorphism, Restriction Fragment Length</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The reduced form of nicotinamide adenine dinucleotide coenzyme Q reductase (complex I) activity has recently been shown to be deficient in the substantia nigra of patients dying with Parkinson's disease. This biochemical defect is identical to that produced by the neurotoxin 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP), which also produces parkinsonism in humans. Complex I comprises 25 polypeptides, seven of which are encoded by mitochondrial DNA. Restriction fragment analysis of substantia nigra DNA from six patients with Parkinson's disease did not show any major deletion. In two cases, there were different novel polymorphisms that were not observed in control brain (n = 6) or blood (n = 34) samples.</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="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name></region><name sortKey="Harding, A E" sort="Harding, A E" uniqKey="Harding A" first="A. E." last="Harding">A. E. Harding</name><name sortKey="Holt, I J" sort="Holt, I J" uniqKey="Holt I" first="I. J." last="Holt">I. J. Holt</name><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P." last="Jenner">P. Jenner</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="Sweeney, M" sort="Sweeney, M" uniqKey="Sweeney M" first="M." last="Sweeney">M. Sweeney</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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