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LRRK2 links genetic and sporadic Parkinson's disease

Kluss, Jillian H., Mamais, Adamantios, Cookson, Mark R.·2019·Biochemical Society Transactions
DOI 10.1042/bst20180462PMC PMC6563926
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Abstract

The past two decades in research has revealed the importance of leucine-rich repeat kinase 2 (LRRK2) in both monogenic and sporadic forms of Parkinson's disease (PD). In families, mutations in LRRK2 can cause PD with age-dependent but variable penetrance and genome-wide association studies have found variants of the gene that are risk factors for sporadic PD. Functional studies have suggested that the common mechanism that links all disease-associated variants is that they increase LRRK2 kinase activity, albeit in different ways. Here, we will discuss the roles of LRRK2 in areas of inflammation and vesicular trafficking in the context of monogenic and sporadic PD. We will also provide a hypothetical model that links inflammation and vesicular trafficking together in an effort to outline how these pathways might interact and eventually lead to neuronal cell death. We will also highlight the translational potential of LRRK2-specific kinase inhibitors for the treatment of PD.

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  • Mutations in the LRRK2 gene are a common cause of familial Parkinson's disease and are also observed in sporadic Parkinson's disease patients.

    “Mutations in the LRRK2 gene are a common cause of familial Parkinson’s disease (PD) and are also observed in sporadic PD patients, indicating a key role for LRRK2 across the entire disease spectrum [1,2,3].”

    From Distinct Roles for RAB10 and RAB29 in Pathogenic LRRK2-Mediated Endolysosomal Trafficking Alterations (2020) · cites this paper as [3]

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Metadata

Authors
Kluss, J. H., Mamais, A., & Cookson, M. R.
Affiliations
Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bldg. 35, 35 Convent Drive, Bethesda, MD 20892-3707, U.S.A.
ORCID
Cookson, Mark R.
Venue
Biochemical Society Transactions
Publisher
Portland Press Ltd.
Published
2019-03-05
Volume
47
Issue
2
Pages
651-661
ISSN
  • 0300-5127
  • 1470-8752
DOI
10.1042/bst20180462
PMC
PMC6563926
Cited by
221
References
5
Language
en

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