Abstract
In this issue of Neuron, Lin et al. report that LRRK2 modulates age-related neurodegeneration caused by overexpression of alpha-synuclein in the forebrain of transgenic mice. Overexpression of LRRK2 accelerates the progression of alpha-synuclein-mediated neuropathological changes, whereas deletion of LRRK2 alleviates these alterations. The results reveal an interesting interaction between alpha-synuclein and LRRK2, two gene products linked to dominantly inherited Parkinson's disease.
2009 Elsevier Inc. All rights reserved.
MeSH terms
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Animals
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Brain / metabolism*
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Brain / pathology
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Brain / physiopathology
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Disease Models, Animal
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Endoplasmic Reticulum / genetics
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Endoplasmic Reticulum / metabolism
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Endoplasmic Reticulum / pathology
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Gene Expression Regulation / genetics
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Genetic Predisposition to Disease / genetics*
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Golgi Apparatus / genetics
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Golgi Apparatus / metabolism
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Golgi Apparatus / pathology
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Humans
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Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
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Mice
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Mice, Transgenic / genetics
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Microtubules / genetics
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Microtubules / metabolism
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Microtubules / pathology
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Nerve Degeneration / genetics
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Nerve Degeneration / metabolism
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Nerve Degeneration / physiopathology
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Parkinson Disease / genetics*
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Parkinson Disease / metabolism*
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Parkinson Disease / physiopathology
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Protein Serine-Threonine Kinases / genetics*
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Protein Transport / genetics
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alpha-Synuclein / genetics*
Substances
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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