MITOCHONDRIAL-DNA ANALYSIS IN PARKINSONS-DISEASE

被引：97

作者：

SCHAPIRA, AHV

HOLT, IJ

SWEENEY, M

HARDING, AE

JENNER, P

MARSDEN, CD

机构：

[1] Department of Neurological Science, Royal Free Hospital School of Medicine, Pharmacology Group, Biomedical Science Division, King's College Hospital, London

[2] University Department of Clinical Neurology, Institute of Neurology, Pharmacology Group, Biomedical Science Division, King's College Hospital, London

[3] Parkinson's Disease Society Experimental Research Laboratories, Pharmacology Group, Biomedical Science Division, King's College Hospital, London

来源：

MOVEMENT DISORDERS | 1990年 / 5卷 / 04期

关键词：

Complex I; DNA; Mitochondria; Parkinson's disease;

D O I：

10.1002/mds.870050406

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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. Copyright © 1990 Movement Disorder Society

引用

页码：294 / 297

页数：4

共 24 条

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