期刊
JOURNAL OF NEUROSCIENCE
卷 26, 期 15, 页码 3942-3950出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4965-05.2006
关键词
aggregation; behavior; tyrosine hydroxylase; fibril; dopamine; nigrostriatal; Parkinson; alpha-synuclein
资金
- MRC [MC_U105184291] Funding Source: UKRI
- Medical Research Council [MC_U105184291] Funding Source: researchfish
- Medical Research Council [MC_U105184291] Funding Source: Medline
- NIA NIH HHS [P30 AG10133] Funding Source: Medline
- Parkinson's UK [G-4039] Funding Source: Medline
Dysfunction of the 140 aa protein alpha-synuclein plays a central role in Lewy body disorders, including Parkinson's disease, as well as in multiple system atrophy. Here, we show that the expression of truncated human alpha-synuclein(1-120), driven by the rat tyrosine hydroxylase promoter on a mouse alpha-synuclein null background, leads to the formation of pathological inclusions in the substantia nigra and olfactory bulb and to a reduction in striatal dopamine levels. At the behavioral level, the transgenic mice showed a progressive reduction in spontaneous locomotion and an increased response to amphetamine. These findings suggest that the C-terminal of alpha-synuclein is an important regulator of aggregation in vivo and will help to understand the mechanisms underlying the pathogenesis of Lewy body disorders and multiple system atrophy.
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