Summary
Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.
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Mytilineou, C., Werner, P., Molinari, S. et al. Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease. J Neural Transm Gen Sect 8, 223–228 (1994). https://doi.org/10.1007/BF02260943
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DOI: https://doi.org/10.1007/BF02260943