Journal
JOURNAL OF NEUROSCIENCE
Volume 31, Issue 3, Pages 907-912Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5092-10.2011
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Funding
- Michael J. Fox Foundation for Parkinson's Research
- Max Planck Society
- Swiss National Science Foundation [310030_127478]
- Ecole Polytechnique Federale de Lausanne
- Swiss National Science Foundation (SNF) [310030_127478] Funding Source: Swiss National Science Foundation (SNF)
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The G2019S mutation in the leucine-rich repeat kinase 2 (LRRK2) gene is the most common genetic cause of Parkinson's disease (PD), accounting for a significant proportion of both autosomal dominant familial and sporadic PD cases. Our aim in the present study is to generate a mammalian model of mutant G2019S LRRK2 pathogenesis, which reproduces the robust nigral neurodegeneration characteristic of PD. We developed adenoviral vectors to drive neuron-specific expression of full-length wild-type or mutant G2019S human LRRK2 in the nigrostriatal system of adult rats. Wild-type LRRK2 did not induce any significant neuronal loss. In contrast, under the same conditions and levels of expression, G2019S mutant LRRK2 causes a progressive degeneration of nigral dopaminergic neurons. Our data provide a novel rat model of PD, based on a prevalent genetic cause, that reproduces a cardinal feature of the disease within a rapid time frame suitable for testing of neuroprotective strategies.
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