Selenomethionine reduces the deposition of beta-amyloid plaques by modulating beta-secretase and enhancing selenoenzymatic activity in a mouse model of alzheimer's disease | |
Zhang, Zhong-Hao1; Chen, Chen2; Wu, Qiu-Yan2; Zheng, Rui2; Liu, Qiong2; Ni, Jia-Zuan1,2; Hoffmann, Peter R.3; Song, Guo-Li2 | |
刊名 | Metallomics |
2016-08-01 | |
卷号 | 8期号:8页码:782-789 |
ISSN号 | 1756-5901 |
DOI | 10.1039/c6mt00117c |
通讯作者 | Song, guo-li(lilys@szu.edu.cn) |
英文摘要 | 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. |
WOS关键词 | INTRANEURONAL A-BETA ; OXIDATIVE STRESS ; SELENOPROTEIN-P ; TRANSGENIC MICE ; TAU PATHOLOGY ; CASCADE HYPOTHESIS ; COGNITIVE DECLINE ; IN-VIVO ; SELENIUM ; NEURODEGENERATION |
WOS研究方向 | Biochemistry & Molecular Biology |
WOS类目 | Biochemistry & Molecular Biology |
语种 | 英语 |
出版者 | ROYAL SOC CHEMISTRY |
WOS记录号 | WOS:000381416600007 |
内容类型 | 期刊论文 |
URI标识 | http://www.corc.org.cn/handle/1471x/2375617 |
专题 | 中国科学院大学 |
通讯作者 | Song, Guo-Li |
作者单位 | 1.Univ Chinese Acad Sci, Chinese Acad Sci, Changchun Inst Appl Chem, Changchun, Peoples R China 2.Shenzhen Univ, Shenzhen Key Lab Marine Bioresources & Ecol, Coll Life Sci & Oceanog, Shenzhen, Peoples R China 3.Univ Hawaii, John A Burns Sch Med, Dept Cell & Mol Biol, Honolulu, HI 96822 USA |
推荐引用方式 GB/T 7714 | Zhang, Zhong-Hao,Chen, Chen,Wu, Qiu-Yan,et al. Selenomethionine reduces the deposition of beta-amyloid plaques by modulating beta-secretase and enhancing selenoenzymatic activity in a mouse model of alzheimer's disease[J]. Metallomics,2016,8(8):782-789. |
APA | Zhang, Zhong-Hao.,Chen, Chen.,Wu, Qiu-Yan.,Zheng, Rui.,Liu, Qiong.,...&Song, Guo-Li.(2016).Selenomethionine reduces the deposition of beta-amyloid plaques by modulating beta-secretase and enhancing selenoenzymatic activity in a mouse model of alzheimer's disease.Metallomics,8(8),782-789. |
MLA | Zhang, Zhong-Hao,et al."Selenomethionine reduces the deposition of beta-amyloid plaques by modulating beta-secretase and enhancing selenoenzymatic activity in a mouse model of alzheimer's disease".Metallomics 8.8(2016):782-789. |
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