Sodium selenate activated Wnt/ β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease.

Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease.
Exp Neurol. 2017 Jul 12;:
Authors: Jin N, Zhu H, Liang X, Huang W, Xie Q, Xiao P, Ni J, Liu Q
Abstract
Accumulating evidences show that selenium dietary intake is inversely associated with the mortality of Alzheimer's disease (AD). Sodium selenate has been reported to reduce neurofibrillary tangles (NFT) in the tauopathic mouse models, but its effects on the Wnt/β-catenin signaling pathway and APP processing remain unknown during AD formation. In this paper, triple transgenic AD mice (3×Tg-AD) had been treated with sodium selenate in drinking water for 10month before the detection of hippocampal pathology. Increased Aβ generation, tau hyperphosphorylation and neuronal apoptosis were found in the hippocampus of AD model mouse. Down-regulation of Wnt/β-catenin signaling is closely associated with the alteration of AD pathology. Treatment with sodium selenate significantly promoted the activity of protein phosphatases of type 2A (PP2A) and repressed the hallmarks of AD. Activation of PP2A by sodium selenate could increase active β-catenin level and inhibit GSK3β activity in the hippocampal tissue and primarily cultured neurons of AD model mouse, leading to activation of Wnt/β-catenin signaling and transactivation of target genes, including positively-regulated genes c-myc, survivin, TXNR...

Source: Experimental Neurology - July 12, 2017 Category: Neurology Authors: Jin N, Zhu H, Liang X, Huang W, Xie Q, Xiao P, Ni J, Liu Q Tags: Exp Neurol Source Type: research