期刊
NEURON
卷 64, 期 6, 页码 771-773出版社
CELL PRESS
DOI: 10.1016/j.neuron.2009.12.017
关键词
-
资金
- 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
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据
分享论文
