期刊
METALLOMICS
卷 8, 期 8, 页码 782-789出版社
ROYAL SOC CHEMISTRY
DOI: 10.1039/c6mt00117c
关键词
-
资金
- National Natural Science Foundation of China [81400847, 31470804, 21271131]
- Grants of Shenzhen Municipal Science and Technology Industry and Information Technology Commission Research [JCYJ20150529164656093, JSGG20140703163838793]
Alzheimer's disease (AD) is characterized by the production of large amounts of beta-amyloid (Ab) and the accumulation of extracellular senile plaques, which have been considered to be potential targets in the treatment of AD. Selenium (Se) is a nutritionally essential trace element with known antioxidant potential and Se status has been shown to decrease with age and has a close relationship with cognitive competence in AD. Selenomethionine (Se-Met), a major reserve form of Se in organisms, has been shown in our previous study to ameliorate the decline in cognitive function, increase oxidation resistance, and reduce tau hyperphosphorylation in a triple transgenic mouse model of AD. However, it has not been reported whether Se-Met has any effects on A beta pathology in AD mice. To study the effect of Se-Met on A beta pathology and the function of selenoproteins/selenoenzymes in 3x Tg-AD mice, 3x Tg-AD mice at 8 months of age were treated with Se-Met for 3 months. Se-Met led to significantly reduced production and deposition of A beta, down-regulation of beta-secretase levels and enhanced activity of selenoenzymes as well as increased levels of Se in the hippocampus and cortex. Se-Met reduces amyloidogenic processing of amyloid precursor protein while modulating beta-secretase and selenoenzymatic activity in AD mice. These results indicate that Se-Met might exert its therapeutic effect through multiple pathways in AD.
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