Abstract
In this review I outline the arguments as to whether we should consider Parkinson disease one or more than one entity and discuss genetic findings from Mendelian and whole-genome association analysis in that context. I discuss what the demonstration of disease spread implies for our analysis of the genetic and epidemiologic risk factors for disease and outline the surprising fact that we now have genetically identified on the order of half our risk for developing the disease.
Copyright © 2010 Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Genetic Predisposition to Disease*
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Genome-Wide Association Study / methods*
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Humans
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Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
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Parkinson Disease / epidemiology*
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Parkinson Disease / etiology
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Parkinson Disease / genetics*
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Parkinson Disease / pathology
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Protein Serine-Threonine Kinases / genetics
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Risk Factors
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alpha-Synuclein / genetics
Substances
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SNCA protein, human
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alpha-Synuclein
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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