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González-Rodríguez, Patricia; Zampese, Enrico; Stout, Kristen A; Guzman, Jaime N; Ilijic, Ema; Yang, Ben; Tkatch, Tatiana; Stavarache, Mihaela A; Wokosin, David L; Gao, Lin; Kaplitt, Michael G; López-Barneo, José; Schumacker, Paul T; Surmeier, D James
Nature (London), 11/2021, Letnik: 599, Številka: 7886Journal Article
Loss of functional mitochondrial complex I (MCI) in the dopaminergic neurons of the substantia nigra is a hallmark of Parkinson's disease . Yet, whether this change contributes to Parkinson's disease pathogenesis is unclear . Here we used intersectional genetics to disrupt the function of MCI in mouse dopaminergic neurons. Disruption of MCI induced a Warburg-like shift in metabolism that enabled neuronal survival, but triggered a progressive loss of the dopaminergic phenotype that was first evident in nigrostriatal axons. This axonal deficit was accompanied by motor learning and fine motor deficits, but not by clear levodopa-responsive parkinsonism-which emerged only after the later loss of dopamine release in the substantia nigra. Thus, MCI dysfunction alone is sufficient to cause progressive, human-like parkinsonism in which the loss of nigral dopamine release makes a critical contribution to motor dysfunction, contrary to the current Parkinson's disease paradigm .
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