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Article Publish Status: FREE
Abstract Title:

Magnesium Ions Inhibit the Expression of Tumor Necrosis Factorα and the Activity of γ-Secretase in a β-Amyloid Protein-Dependent Mechanism in APP/PS1 Transgenic Mice.

Abstract Source:

Front Mol Neurosci. 2018 ;11:172. Epub 2018 May 30. PMID: 29899688

Abstract Author(s):

Xin Yu, Pei-Pei Guan, Di Zhu, Yun-Yue Liang, Tao Wang, Zhan-You Wang, Pu Wang

Article Affiliation:

Xin Yu

Abstract:

Alzheimer's disease (AD) is a neurodegenerative disease characterized by cognitive impairment. The neuropathological features of AD are the aggregation of extracellular amyloidβ-protein (Aβ) and tau phosphorylation. Recently, AD was found to be associated with magnesium ion (Mg) deficit and tumor necrosis factor-alpha (TNF-α) elevation in the serum or brains of AD patients. To study the relationship between Mgand TNF-α, we used human- or mouse-derived glial and neuronal cell lines or APP/PS1 transgenic (Tg) mice asandexperimental models, respectively. Our data demonstrates that magnesium-L-threonate (MgT) can decrease the expression of TNF-α by restoring the levels of Mgin glial cells. In addition, PI3-K/AKT and NF-κB signals play critical roles in mediating the effects of Mgon suppressing the expression of TNF-α. In neurons, Mgelevation showed similar suppressive effects on the expression of presenilin enhancer 2 (PEN2) and nicastrin (NCT) through a PI3-K/AKT and NF-κB-dependent mechanism. As the major components of γ-secretase, overexpression of presenilin 1 (PS1), PEN2 and NCT potentially promote the synthesis of Aβ, which in turn activates TNF-α in glial cells. Reciprocally, TNF-α stimulates the expression of PEN2 and NCT in neurons. The crosstalk between TNF-α and Aβ in glial cells and neurons could ultimately aggravate the development and progression of AD.

Study Type : In Vitro Study, Transgenic Animal Study

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