Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease
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 A...
Ausführliche Beschreibung
Autor*in: |
Jin, Na [verfasserIn] |
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E-Artikel |
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Englisch |
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2017transfer abstract |
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14 |
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Übergeordnetes Werk: |
Enthalten in: Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation - Xu, Chao ELSEVIER, 2022, a journal of neuroscience research, Amsterdam [u.a.] |
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Übergeordnetes Werk: |
volume:297 ; year:2017 ; pages:36-49 ; extent:14 |
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DOI / URN: |
10.1016/j.expneurol.2017.07.006 |
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ELV036170216 |
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245 | 1 | 0 | |a Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
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520 | |a 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. | ||
520 | |a 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. | ||
700 | 1 | |a Zhu, Huazhang |4 oth | |
700 | 1 | |a Liang, Xiao |4 oth | |
700 | 1 | |a Huang, Wei |4 oth | |
700 | 1 | |a Xie, Qingguo |4 oth | |
700 | 1 | |a Xiao, Peng |4 oth | |
700 | 1 | |a Ni, Jiazuan |4 oth | |
700 | 1 | |a Liu, Qiong |4 oth | |
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10.1016/j.expneurol.2017.07.006 doi GBVA2017020000027.pica (DE-627)ELV036170216 (ELSEVIER)S0014-4886(17)30180-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 630 640 VZ 48.30 bkl Jin, Na verfasserin aut Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease 2017transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. Zhu, Huazhang oth Liang, Xiao oth Huang, Wei oth Xie, Qingguo oth Xiao, Peng oth Ni, Jiazuan oth Liu, Qiong oth Enthalten in Elsevier Xu, Chao ELSEVIER Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation 2022 a journal of neuroscience research Amsterdam [u.a.] (DE-627)ELV008416567 volume:297 year:2017 pages:36-49 extent:14 https://doi.org/10.1016/j.expneurol.2017.07.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 48.30 Natürliche Ressourcen Land- und Forstwirtschaft VZ AR 297 2017 36-49 14 045F 610 |
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10.1016/j.expneurol.2017.07.006 doi GBVA2017020000027.pica (DE-627)ELV036170216 (ELSEVIER)S0014-4886(17)30180-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 630 640 VZ 48.30 bkl Jin, Na verfasserin aut Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease 2017transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. Zhu, Huazhang oth Liang, Xiao oth Huang, Wei oth Xie, Qingguo oth Xiao, Peng oth Ni, Jiazuan oth Liu, Qiong oth Enthalten in Elsevier Xu, Chao ELSEVIER Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation 2022 a journal of neuroscience research Amsterdam [u.a.] (DE-627)ELV008416567 volume:297 year:2017 pages:36-49 extent:14 https://doi.org/10.1016/j.expneurol.2017.07.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 48.30 Natürliche Ressourcen Land- und Forstwirtschaft VZ AR 297 2017 36-49 14 045F 610 |
allfields_unstemmed |
10.1016/j.expneurol.2017.07.006 doi GBVA2017020000027.pica (DE-627)ELV036170216 (ELSEVIER)S0014-4886(17)30180-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 630 640 VZ 48.30 bkl Jin, Na verfasserin aut Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease 2017transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. Zhu, Huazhang oth Liang, Xiao oth Huang, Wei oth Xie, Qingguo oth Xiao, Peng oth Ni, Jiazuan oth Liu, Qiong oth Enthalten in Elsevier Xu, Chao ELSEVIER Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation 2022 a journal of neuroscience research Amsterdam [u.a.] (DE-627)ELV008416567 volume:297 year:2017 pages:36-49 extent:14 https://doi.org/10.1016/j.expneurol.2017.07.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 48.30 Natürliche Ressourcen Land- und Forstwirtschaft VZ AR 297 2017 36-49 14 045F 610 |
allfieldsGer |
10.1016/j.expneurol.2017.07.006 doi GBVA2017020000027.pica (DE-627)ELV036170216 (ELSEVIER)S0014-4886(17)30180-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 630 640 VZ 48.30 bkl Jin, Na verfasserin aut Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease 2017transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. Zhu, Huazhang oth Liang, Xiao oth Huang, Wei oth Xie, Qingguo oth Xiao, Peng oth Ni, Jiazuan oth Liu, Qiong oth Enthalten in Elsevier Xu, Chao ELSEVIER Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation 2022 a journal of neuroscience research Amsterdam [u.a.] (DE-627)ELV008416567 volume:297 year:2017 pages:36-49 extent:14 https://doi.org/10.1016/j.expneurol.2017.07.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 48.30 Natürliche Ressourcen Land- und Forstwirtschaft VZ AR 297 2017 36-49 14 045F 610 |
allfieldsSound |
10.1016/j.expneurol.2017.07.006 doi GBVA2017020000027.pica (DE-627)ELV036170216 (ELSEVIER)S0014-4886(17)30180-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 630 640 VZ 48.30 bkl Jin, Na verfasserin aut Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease 2017transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. 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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. Zhu, Huazhang oth Liang, Xiao oth Huang, Wei oth Xie, Qingguo oth Xiao, Peng oth Ni, Jiazuan oth Liu, Qiong oth Enthalten in Elsevier Xu, Chao ELSEVIER Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation 2022 a journal of neuroscience research Amsterdam [u.a.] (DE-627)ELV008416567 volume:297 year:2017 pages:36-49 extent:14 https://doi.org/10.1016/j.expneurol.2017.07.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 48.30 Natürliche Ressourcen Land- und Forstwirtschaft VZ AR 297 2017 36-49 14 045F 610 |
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sodium selenate activated wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of alzheimer's disease |
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Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. |
abstractGer |
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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. |
abstract_unstemmed |
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, TXNRD2 and negatively-regulated gene BACE1. Meanwhile, APP phosphorylation was also reduced on the Thr668 residue after selenate treatment, causing the decreases of APP cleavage and Aβ generation. These findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment. |
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Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
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