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Genetics

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Investigating Convergent Actions of Genes Linked to Familial Parkinson’s Disease

Wolozin B. · Saha S. · Guillily M. · Ferree A. · Riley M.

Author affiliations

Department of Pharmacology, Boston University School of Medicine, Boston, Mass., USA

Corresponding Author

Prof. Benjamin Wolozin, MD, PhD

Department of Pharmacology, Boston University School of Medicine

715 Albany St., R614

Boston, MA 02118-2526 (USA)

Tel. +1 617 414 2652, Fax +1 617 414 2651, E-Mail bwolozin@bu.edu

Related Articles for ""

Neurodegenerative Dis 2008;5:182–185

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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


Article / Publication Details

First-Page Preview
Abstract of Genetics

Published online: March 06, 2008
Issue release date: March 2008

Number of Print Pages: 4
Number of Figures: 1
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


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