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.
Publication types
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Research Support, N.I.H., Intramural
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Review
MeSH terms
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Central Nervous System / metabolism
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Central Nervous System / pathology
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Dopamine / metabolism
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Genetic Predisposition to Disease* / genetics
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Humans
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Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
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Models, Biological
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Mutation / genetics*
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Parkinson Disease / genetics
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Parkinson Disease / metabolism*
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Parkinson Disease / pathology
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism*
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Risk Factors
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alpha-Synuclein / metabolism
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tau Proteins / metabolism
Substances
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alpha-Synuclein
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tau Proteins
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LRRK2 protein, human
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Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
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Protein Serine-Threonine Kinases
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Dopamine