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Neurodegener Dis. 2008;5(3-4):182-5. doi: 10.1159/000113697. Epub 2008 Mar 6.

Investigating convergent actions of genes linked to familial Parkinson's disease.

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  • 1Department of Pharmacology, Boston University School of Medicine, Boston, Mass. 02118-2526, USA. bwolozin@bu.edu

Abstract

BACKGROUND:

Mutations in LRRK2 are among the most frequent genetic changes identified in Parkinson's disease (PD), but how LRRK2 contributes to the pathophysiology of PD is not known.

OBJECTIVES:

To investigate how expressing wild-type or G2019S LRRK2 modifies cellular responses to rotenone, a mitochondrial toxin.

METHODS:

We investigated the vulnerability to mitochondrial toxins in Caenorhabditis elegans expressing wild-type or G2019S LRRK2.

RESULTS:

We observed a powerful role for LRRK2 in mitochondrial biology. Overexpressing LRRK2 strongly protects C. elegans against rotenone toxicity. The G2019S LRRK2 construct also protected LRRK2 against rotenone, but to a lesser degree than wild-type LRRK2. Knockdown of lrk-1 potentiated rotenone toxicity.

CONCLUSIONS:

These data suggest that LRRK1/2 regulate mitochondrial physiology.

2008 S. Karger AG, Basel

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