Exposure to Pyrithiamine Increases beta-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain
文献类型：期刊论文
| 作者 | Zhao, Jing ; Sun, Xiaojing ; Yu, Zhe ; Pan, Xiaoli ; Gu, Fenghua ; Chen, Jia ; Dong, Wenxin ; Zhao, Lei ; Zhong, Chunjiu |
| 刊名 | NEUROTOXICITY RESEARCH
 |
| 出版日期 | 2011 |
| 卷号 | 19期号:4页码:575-583 |
| 关键词 | Alzheimer's disease Thiamine deficiency Pyrithiamine Glycogen synthase kinase-3 POSITRON-EMISSION-TOMOGRAPHY FAMILIAL ALZHEIMERS-DISEASE THIAMINE-DEPENDENT ENZYMES TRANSGENIC MICE WERNICKES ENCEPHALOPATHY INSULIN-RESISTANCE PRECURSOR PROTEIN MOUSE MODELS A-BETA DEFICIENCY |
| ISSN号 | 1029-8428 |
| 通讯作者 | Zhong, CJ (reprint author), Fudan Univ, Zhongshan Hosp, Dept Neurol, Shanghai 200032, Peoples R China,zhongcj@163.com |
| 英文摘要 | Decreased thiamine-dependent enzyme activity and/or thiamine deficiency (TD) have been linked to Alzheimer's disease (AD). In this study, we administered pyrithiamine, an anti-thiamine compound, to both APP/PS1 transgenic mice and wild-type littermate control mice; alternatively, we induced TD by thiamine-depleted diet. Pyrithiamine treatment and diet-induced TD impaired the memory of wild-type mice, but had little effect on APP/PS1 mice. Pathophysiologically, pyrithiamine treatment and diet-induced TD aggravated beta-amyloid accumulation in the brain. This was demonstrated by increased beta-amyloid in the brains of wild-type mice using ELISA and by the number of amyloid plaques in the brains of APP/PS1 transgenic mice using immunochemical staining. Also, enhanced numbers of phosphorylated Tau-positive cells were observed in both APP/PS1 transgenic and wild-type mice. Furthermore, pyrithiamine decreased the phosphorylation rates of glycogen synthase kinase (GSK)-3 beta and raised its enzymatic activity, but had little influence on GSK-3 alpha. Diet-induced TD reduced the phosphorylated rates and increased the activities of GSK-3, GSK-3 alpha, and GSK-3 beta. These results suggest that when sufficient thiamine supplement is administered, pyrithiamine can cause AD-like pathological alterations similar to that of diet-induced TD. |
| 学科主题 | Neurosciences & Neurology |
| 收录类别 | SCI |
| 资助信息 | Science and Technology Commission of Shanghai Municipality[09DZ1950400, 10430709600] |
| 语种 | 英语 |
| 公开日期 | 2012-07-13 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/1543]  |
| 专题 | 上海神经科学研究所_神经所(总) |
| 推荐引用方式 GB/T 7714 | Zhao, Jing,Sun, Xiaojing,Yu, Zhe,et al. Exposure to Pyrithiamine Increases beta-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain[J]. NEUROTOXICITY RESEARCH,2011,19(4):575-583. |
| APA | Zhao, Jing.,Sun, Xiaojing.,Yu, Zhe.,Pan, Xiaoli.,Gu, Fenghua.,...&Zhong, Chunjiu.(2011).Exposure to Pyrithiamine Increases beta-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain.NEUROTOXICITY RESEARCH,19(4),575-583. |
| MLA | Zhao, Jing,et al."Exposure to Pyrithiamine Increases beta-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain".NEUROTOXICITY RESEARCH 19.4(2011):575-583. |
入库方式： OAI收割
来源：上海神经科学研究所
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