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The role of leucine-rich repeat kinase 2 (LRRK2) in Parkinson's disease

Nature Reviews Neuroscience volume 11, pages 791–797 (2010)Cite this article

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Abstract

Parkinson's disease, like many common age-related conditions, is now recognized to have a substantial genetic component. Here, I discuss how mutations in a large complex gene — leucine-rich repeat kinase 2 (LRRK2) — affect protein function, and I review recent evidence that LRRK2 mutations affect pathways that involve other proteins that have been implicated in Parkinson's disease, specifically α-synuclein and tau. These concepts can be used to understand disease processes and to develop therapeutic opportunities for the treatment of Parkinson's disease.

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Figure 1: Domains and mutations of LRRK2.
Figure 2: LRRK2, α-synuclein and tau.

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Acknowledgements

I would like to thank E. Greggio and J.-M. Taymans for critically reading the manuscript. This research was supported by the Intramural Research Program of the National Institutes of Health (NIH), National Institute on Aging.

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  1. Mark R. Cookson is at the Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health (NIH), Building 35, Room 1A116, MSC 3707, 35 Convent Drive, Bethesda, Maryland 20982-3707, USA. Cookson@mail.nih.gov,

    Mark R. Cookson

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Cookson, M. The role of leucine-rich repeat kinase 2 (LRRK2) in Parkinson's disease. Nat Rev Neurosci 11, 791–797 (2010). https://doi.org/10.1038/nrn2935

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