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pubmed-article:8359498pubmed:abstractTextThe precise relationship of the complex I deficiency in PD to the dopaminergic cell death and aetiology of this disorder is as yet unknown. However, evidence is accruing that this mitochondrial defect may play a central role in the cascade of events that terminates in nigral neuronal loss. Further work needs to be carried out to determine the molecular mechanisms that underlie the complex I deficiency as these may provide important indicators to the ultimate cause of PD. This may involve a genetic abnormality of complex I that may convey a susceptibility to developing PD. Alternatively, exogenous or endogenous toxic agents may target nigral complex I along pathways similar to those recognized for MPTP. A combination of a genetic predisposition in addition to an environmental precipitant has gained substantial support as an explanation for the cause of PD.lld:pubmed
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pubmed-article:8359498pubmed:articleTitleFree radicals and mitochondrial dysfunction in Parkinson's disease.lld:pubmed
pubmed-article:8359498pubmed:affiliationDepartment of Neuroscience, Royal Free Hospital School of Medicine, London, U.K.lld:pubmed
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