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Table of Contents
Vol. 16, No. 1, 2008
Issue release date: December 2007
Section title: Paper
Neurosignals 2008;16:99–105

Mutations in LRRK2 as a Cause of Parkinson’s Disease

Giasson B.I.a · Van Deerlin V.M.b
Departments of aPharmacology and bPathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pa., USA
email Corresponding Author

Dr. Benoit I. Giasson

Department of Pharmacology, University of Pennsylvania School of Medicine

3620 Hamilton Walk, 125 John Morgan Building

Philadelphia, PA 19104-6084 (USA)

Tel. +1 215 573 6012, Fax +1 215 573 2236, E-Mail giassonb@mail.med.upenn.edu

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Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common known cause of late-onset Parkinson’s disease (PD). Clinical and pathological studies have demonstrated that in the majority of cases LRRK2 mutations lead to PD with classical clinical and pathological features. However, in some patients the pathological features can be distinct and/or more extensive than typically seen in PD. Collectively, these findings provide important clues into the mechanisms by which LRRK2 mutations can lead to demise of dopaminergic neurons. The understanding of LRRK2 protein function and its gene regulation and the consequences of mutations are still at their infancy, but scientific findings are progressing at a rapid pace. Although more detailed information on LRRK2 is still needed in the quest for therapeutic intervention that could halt or slow the progression of disease, here we summarize the current information on the biological and pathological properties of LRRK2.

© 2008 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: December 05, 2007
Issue release date: December 2007

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 0

ISSN: 1424-862X (Print)
eISSN: 1424-8638 (Online)

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

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