IR@PKUHSC  > 北京大学基础医学院  > 神经生物学系
学科主题基础医学
Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer′s disease mouse model
Li, Wei1; Yu, Jia2; Liu, Yong3; Huang, Xiaojie1; Abumaria, Nashat1; Zhu, Ying1; Huang, Xian1; Xiong, Wenxiang1; Ren, Chi1; Liu, Xian-Guo3; Chui, Dehua2; Liu, Guosong1
关键词Alzheimer&prime s disease Brain magnesium Synaptoprotection NMDAR signaling BACE1
刊名MOLECULAR BRAIN
2014-09-13
DOI10.1186/s13041-014-0065-y
7期:1
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]NMDA RECEPTOR TRAFFICKING ; APP TRANSGENIC MICE ; MEMORY DEFICITS ; AMYLOID DEPOSITION ; BETA ; CALCIUM ; PLASTICITY ; MECHANISM ; NEUROPATHOLOGY ; TRANSMITTER
英文摘要

Background: Profound synapse loss is one of the major pathological hallmarks associated with Alzheimer′s disease, which might underlie memory impairment. Our previous work demonstrates that magnesium ion is a critical factor in controlling synapse density/plasticity. Here, we tested whether elevation of brain magnesium, using a recently developed compound (magnesium-L-threonate, MgT), can ameliorate the AD-like pathologies and cognitive deficits in the APPswe/PS1dE9 mice, a transgenic mouse model of Alzheimer′s disease.

Results: MgT treatment reduced A beta-plaque, prevented synapse loss and memory decline in the transgenic mice. Strikingly, MgT treatment was effective even when the treatment was given to the mice at the end-stage of their Alzheimer′s disease-like pathological progression. To explore how elevation of brain magnesium ameliorates the AD-like pathologies in the brain of transgenic mice, we studied molecules critical for APP metabolism and signaling pathways implicated in synaptic plasticity/density. In the transgenic mice, the NMDAR signaling pathway was downregulated, while the BACE1 expression were upregulated. MgT treatment prevented the impairment of these signaling pathways, stabilized BACE1 expression and reduced sAPP beta and beta-CTF in the transgenic mice. At the molecular level, elevation of extracellular magnesium prevented the high A beta-induced reductions in synaptic NMDARs by preventing calcineurin overactivation in hippocampal slices.

Conclusions: Our results suggest that elevation of brain magnesium exerts substantial synaptoprotective effects in a mouse model of Alzheimer′s disease, and hence it might have therapeutic potential for treating Alzheimer′s disease.

语种英语
WOS记录号WOS:000342698800001
引用统计
被引频次:35[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56022
专题北京大学基础医学院_神经生物学系
作者单位1.Tsinghua Univ, Sch Med, Beijing 100084, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Neurosci Res Inst, Beijing 100871, Peoples R China
3.Sun Yat Sen Univ, Zhongshan Sch Med, Dept Physiol, Guangzhou 510275, Guangdong, Peoples R China
推荐引用方式
GB/T 7714
Li, Wei,Yu, Jia,Liu, Yong,等. Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer′s disease mouse model[J]. MOLECULAR BRAIN,2014,7(1).
APA Li, Wei.,Yu, Jia.,Liu, Yong.,Huang, Xiaojie.,Abumaria, Nashat.,...&Liu, Guosong.(2014).Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer′s disease mouse model.MOLECULAR BRAIN,7(1).
MLA Li, Wei,et al."Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer′s disease mouse model".MOLECULAR BRAIN 7.1(2014).
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