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Effect of aging and dopaminomimetic therapy on mitochondrial respiratory function in Parkinson's disease
Author(s) -
Bravi Daniele,
Anderson Jeffrey J.,
Dagani Fiorenzo,
Davis Thomas L.,
Ferrari Rosaria,
Gillespie Marge,
Chase Thomas N.
Publication year - 1992
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.870070307
Subject(s) - parkinson's disease , medicine , degenerative disease , disease , respiratory system , mitochondrial respiratory chain , neuroscience , psychology , mitochondrion , biology , microbiology and biotechnology
Oxygen consumption and enzyme activity were evaluted in platelet mitochondria from 17 patients with Parkinson's disease. In comparison with age‐matched controls, no consistent abnormality could be discerned in complex I, complex II‐III, or complex IV oxygen consumption, or in the enzyme activity of these respiratory chain complexes. Neither chronic therapy with levodopa/carbidopa alone nor in combination with deprenyl significantly affected any measure of mitochondrial respiratory function. There was no discernible relationship between patient age or disease severity and any parameter of mitochondrial respiration. Moreover, blood lactate levels following glucose loading were not different in patients and controls. These results fail to support the occurrence of a generalized defect in any mitochondrial respiratory function in Parkinson's disease.