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September 08, 2015; 85 (10) Editorial

Fruit flies, bile acids, and Parkinson disease

A mitochondrial connection?

J. Timothy Greenamyre, Laurie H. Sanders, Thomas Gasser
First published August 7, 2015, DOI: https://doi.org/10.1212/WNL.0000000000001912
J. Timothy Greenamyre
From the Pittsburgh Institute for Neurodegenerative Diseases and Department of Neurology (J.T.G., L.H.S.), University of Pittsburgh, PA; and the Department of Neurology and Department of Neurodegenerative Diseases (T.G.), Hertie Institute for Clinical Brain Research, University of Tübingen, Germany.
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Laurie H. Sanders
From the Pittsburgh Institute for Neurodegenerative Diseases and Department of Neurology (J.T.G., L.H.S.), University of Pittsburgh, PA; and the Department of Neurology and Department of Neurodegenerative Diseases (T.G.), Hertie Institute for Clinical Brain Research, University of Tübingen, Germany.
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Thomas Gasser
From the Pittsburgh Institute for Neurodegenerative Diseases and Department of Neurology (J.T.G., L.H.S.), University of Pittsburgh, PA; and the Department of Neurology and Department of Neurodegenerative Diseases (T.G.), Hertie Institute for Clinical Brain Research, University of Tübingen, Germany.
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Fruit flies, bile acids, and Parkinson disease
A mitochondrial connection?
J. Timothy Greenamyre, Laurie H. Sanders, Thomas Gasser
Neurology Sep 2015, 85 (10) 838-839; DOI: 10.1212/WNL.0000000000001912

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Parkinson disease (PD) has been strongly associated with systemic defects in mitochondrial function. The best characterized of these is probably reduced activity of complex I of the electron transport chain, which was first reported more than 25 years ago,1 after the discovery of the pro-parkinsonian toxin, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), and its mechanism of action: inhibition of complex I.2 Proof-of-concept that a systemic impairment of complex I can reproduce the selective nigrostriatal degeneration and Lewy pathology of PD came from the rotenone model of PD in rats in 2000.3 Shortly thereafter, it became clear that certain autosomal recessive forms of PD are caused by mutations in genes that affect mitochondrial function or quality control, such as parkin and PINK1. Moreover, both parkin and PINK1 mutations are associated with a loss of complex I activity.4,5

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  • See page 846

  • © 2015 American Academy of Neurology
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