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Background: Mitochondrial disorders may affect basal ganglia function. In add ition, decreased activity of complex I of the mitochondrial electron transport c hain has been linked to the pathogenesis of dopaminergic cell loss in Parkinson ’s disease. Abstract Objective: To investigate the dopaminergic system in patients with known mitochondrial disorders and complex I deficiency. Methods: Dopamine trans porter density was studied in 10 female patients with mitochondrial complex I de ficiency by 123I-FP-CIT (N-β -fluoropropyl-2β -carbomethyl-3β -(4-io-dophenyl)-no- rtropane) SPECT. Results: No differences in 123I -FP-CIT striatal binding ratios were observed and no correlation of the degr ee of complex I deficiency and striatal binding ratios could be detected. Conclu sions: These data argue against the possibility that mitochondrial complex I def iciency by itself is sufficient to elicit dopaminergic cell loss.
In addition ition, decreased activity of complex I of the mitochondrial electron transport c hain has been linked to the pathogenesis of dopaminergic cell loss in Parkinson’s disease. Abstract Objective: To investigate the dopaminergic system in patients with known mitochondrial disorders and complex I deficiency. Methods: Dopamine trans porter density was studied in 10 female patients with mitochondrial complex I de ficiency by 123I-FP-CIT (N-beta -fluoropropyl-2β -carbomethyl-3β- -io-dophenyl) -no- rtropane) SPECT. Results: No differences in 123I -FP-CIT striatal binding ratios were observed and no correlation of the degr ee of complex I deficiency and striatal binding ratios could be detected. Conclu sions: These data argue against the possibility that mitochondrial complex I def iciency by itself is sufficient to elicit dopaminergic cell loss.