No evidence for altered muscle mitochondrial function in Parkinson's disease

• Published in: Journal of neurology, neurosurgery and psychiatry Vol. 56; no. 5; pp. 477 - 480
• Main Authors: Anderson, J J, Bravi, D, Ferrari, R, Davis, T L, Baronti, F, Chase, T N, Dagani, F
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd 01-05-1993; BMJ; BMJ Publishing Group LTD
• Subjects: Adult; Aged; Antiparkinson Agents - therapeutic use; Biological and medical sciences; Brain Diseases - physiopathology; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Humans; Levodopa - therapeutic use; Male; Medical sciences; Middle Aged; Mitochondria, Muscle - enzymology; Mitochondria, Muscle - metabolism; Multienzyme Complexes; NADH Dehydrogenase - metabolism; Neurology; Oxygen Consumption; Parkinson Disease - drug therapy; Parkinson Disease - metabolism; Parkinson Disease - physiopathology; Respiratory Function Tests; Substantia Nigra - enzymology; Substantia Nigra - metabolism; Substantia Nigra - physiopathology; Human; Nervous system diseases; Respiratory chain; Mitochondria; Oxygen consumption; Exploration; Degenerative disease; Striated muscle
• ISSN: 0022-3050; 1468-330X
• DOI: 10.1136/jnnp.56.5.477

Recent reports indicate that reductions in mitochondrial respiratory chain function occur in substantia nigra, platelets, and muscle from patients with Parkinson's disease. To confirm and further characterise the presence of a generally distributed mitochondrial defect, mitochondrial metabolism was evaluated in muscle obtained from subjects with Parkinson's disease and from normal controls. Oxygen consumption rates in muscle mitochondria represented by complex I, complexes II-III, or complex IV did not differ between the two groups. Likewise, activities of rotenone sensitive NADH cytochrome c reductase, succinate cytochrome c reductase, or cytochrome oxidase in muscle mitochondria were not significantly different between Parkinsonian and control subjects. These findings fail to provide support for a generalised defect in mitochondrial function in Parkinson's disease but do not exclude an abnormality in respiratory function confined to the substantia nigra.