Journal
NEURON
Volume 64, Issue 6, Pages 771-773Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2009.12.017
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Funding
- NINDS NIH HHS [R01 NS052745, R01 NS052745-05, P50 NS038375, R01 NS041779-09, R01 NS041779, R01 NS041779-09S1, R01 NS071251, R37 NS071251, P50 NS038375-100003] Funding Source: Medline
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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.
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