Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.

Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning and memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties and synaptic plasticity. Recent studies have demonstrated that the serum and brain magnesium levels are...

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Autores principales:	Zhi-Peng Xu, Li Li, Jian Bao, Zhi-Hao Wang, Juan Zeng, En-Jie Liu, Xiao-Guang Li, Rong-Xi Huang, Di Gao, Meng-Zhu Li, Yao Zhang, Gong-Ping Liu, Jian-Zhi Wang
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/30fa5665abc64e01bef229a6576b74e9
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spelling	oai:doaj.org-article:30fa5665abc64e01bef229a6576b74e92021-11-25T05:58:34ZMagnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.1932-620310.1371/journal.pone.0108645https://doaj.org/article/30fa5665abc64e01bef229a6576b74e92014-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0108645https://doaj.org/toc/1932-6203Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning and memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties and synaptic plasticity. Recent studies have demonstrated that the serum and brain magnesium levels are decreased in AD patients; however, the exact role of magnesium in AD pathogenesis remains unclear. Here, we found that the intraperitoneal administration of magnesium sulfate increased the brain magnesium levels and protected learning and memory capacities in streptozotocin-induced sporadic AD model rats. We also found that magnesium sulfate reversed impairments in long-term potentiation (LTP), dendritic abnormalities, and the impaired recruitment of synaptic proteins. Magnesium sulfate treatment also decreased tau hyperphosphorylation by increasing the inhibitory phosphorylation of GSK-3β at serine 9, thereby increasing the activity of Akt at Ser473 and PI3K at Tyr458/199, and improving insulin sensitivity. We conclude that magnesium treatment protects cognitive function and synaptic plasticity by inhibiting GSK-3β in sporadic AD model rats, which suggests a potential role for magnesium in AD therapy.Zhi-Peng XuLi LiJian BaoZhi-Hao WangJuan ZengEn-Jie LiuXiao-Guang LiRong-Xi HuangDi GaoMeng-Zhu LiYao ZhangGong-Ping LiuJian-Zhi WangPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 9, p e108645 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Zhi-Peng Xu Li Li Jian Bao Zhi-Hao Wang Juan Zeng En-Jie Liu Xiao-Guang Li Rong-Xi Huang Di Gao Meng-Zhu Li Yao Zhang Gong-Ping Liu Jian-Zhi Wang Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.
description	Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning and memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties and synaptic plasticity. Recent studies have demonstrated that the serum and brain magnesium levels are decreased in AD patients; however, the exact role of magnesium in AD pathogenesis remains unclear. Here, we found that the intraperitoneal administration of magnesium sulfate increased the brain magnesium levels and protected learning and memory capacities in streptozotocin-induced sporadic AD model rats. We also found that magnesium sulfate reversed impairments in long-term potentiation (LTP), dendritic abnormalities, and the impaired recruitment of synaptic proteins. Magnesium sulfate treatment also decreased tau hyperphosphorylation by increasing the inhibitory phosphorylation of GSK-3β at serine 9, thereby increasing the activity of Akt at Ser473 and PI3K at Tyr458/199, and improving insulin sensitivity. We conclude that magnesium treatment protects cognitive function and synaptic plasticity by inhibiting GSK-3β in sporadic AD model rats, which suggests a potential role for magnesium in AD therapy.
format	article
author	Zhi-Peng Xu Li Li Jian Bao Zhi-Hao Wang Juan Zeng En-Jie Liu Xiao-Guang Li Rong-Xi Huang Di Gao Meng-Zhu Li Yao Zhang Gong-Ping Liu Jian-Zhi Wang
author_facet	Zhi-Peng Xu Li Li Jian Bao Zhi-Hao Wang Juan Zeng En-Jie Liu Xiao-Guang Li Rong-Xi Huang Di Gao Meng-Zhu Li Yao Zhang Gong-Ping Liu Jian-Zhi Wang
author_sort	Zhi-Peng Xu
title	Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.
title_short	Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.
title_full	Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.
title_fullStr	Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.
title_full_unstemmed	Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.
title_sort	magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic alzheimer's model.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/30fa5665abc64e01bef229a6576b74e9
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Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.

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