A P-31 MAGNETIC-RESONANCE SPECTROSCOPY STUDY OF MITOCHONDRIAL-FUNCTION IN SKELETAL-MUSCLE OF PATIENTS WITH PARKINSONS-DISEASE

Citation
Dj. Taylor et al., A P-31 MAGNETIC-RESONANCE SPECTROSCOPY STUDY OF MITOCHONDRIAL-FUNCTION IN SKELETAL-MUSCLE OF PATIENTS WITH PARKINSONS-DISEASE, Journal of the neurological sciences, 125(1), 1994, pp. 77-81
Citations number
16
Categorie Soggetti
Neurosciences
ISSN journal
0022510X
Volume
125
Issue
1
Year of publication
1994
Pages
77 - 81
Database
ISI
SICI code
0022-510X(1994)125:1<77:APMSSO>2.0.ZU;2-K
Abstract
The activity of complex I of the respiratory chain is decreased in the substantia nigra of patients with Parkinson's disease (PD) but the pr esence of this defect in skeletal muscle is controversial. Therefore, the mitochondrial function of skeletal muscle in patients with PD was investigated in vivo using P-31 magnetic resonance spectroscopy. Resul ts from 7 PD patients, 11 age matched controls and 9 mitochondrial myo pathy patients with proven complex I deficiency were obtained from fin ger flexor muscle at rest, during exercise and in recovery from exerci se. In resting muscle, the patients with mitochondrial myopathy showed a low PCr/ATP ratio, a low phosphorylation potential, a high P-i/PCr ratio and a high calculated free [ADP]. During exercise, stores of hig h energy phosphate were depleted more rapidly than normal, while in re covery, the concentration of phosphocreatine and free ADP returned to pre-exercise values more slowly than normal. In contrast, the patients with PD were not significantly different from normal for any of these variables, and no abnormality of muscle energetics was detected. Thre e of the PD patients also had mitochondrial function assessed biochemi cally in muscle biopsies. No respiratory chain defect was identified i n any of these patients by polarography or enzyme analysis when compar ed with age-matched controls. These results suggest that skeletal musc le is not a suitable tissue for the investigation and identification o f the biochemical basis of the nigral complex I deficiency in PD.