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Deprecated: Implicit conversion from float 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Front+Mol+Neurosci 2018 ; 11 (ä): ä Nephropedia Template TP
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Magnesium Ions Inhibit the Expression of Tumor Necrosis Factor ? and the Activity of ?-Secretase in a ?-Amyloid Protein-Dependent Mechanism in APP/PS1 Transgenic Mice #MMPMID29899688
Yu X; Guan PP; Zhu D; Liang YY; Wang T; Wang ZY; Wang P
Front Mol Neurosci 2018[]; 11 (ä): ä PMID29899688show ga
Alzheimer?s disease (AD) is a neurodegenerative disease characterized by cognitive impairment. The neuropathological features of AD are the aggregation of extracellular amyloid ?-protein (A?) and tau phosphorylation. Recently, AD was found to be associated with magnesium ion (Mg2+) deficit and tumor necrosis factor-alpha (TNF-?) elevation in the serum or brains of AD patients. To study the relationship between Mg2+ and TNF-?, we used human- or mouse-derived glial and neuronal cell lines or APP/PS1 transgenic (Tg) mice as in vitro and in vivo experimental models, respectively. Our data demonstrates that magnesium-L-threonate (MgT) can decrease the expression of TNF-? by restoring the levels of Mg2+ in glial cells. In addition, PI3-K/AKT and NF-?B signals play critical roles in mediating the effects of Mg2+ on suppressing the expression of TNF-?. In neurons, Mg2+ elevation showed similar suppressive effects on the expression of presenilin enhancer 2 (PEN2) and nicastrin (NCT) through a PI3-K/AKT and NF-?B-dependent mechanism. As the major components of ?-secretase, overexpression of presenilin 1 (PS1), PEN2 and NCT potentially promote the synthesis of A?, which in turn activates TNF-? in glial cells. Reciprocally, TNF-? stimulates the expression of PEN2 and NCT in neurons. The crosstalk between TNF-? and A? in glial cells and neurons could ultimately aggravate the development and progression of AD.