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
Gespeichert in:
| Autor*in: |
Jin, Na [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
|---|
| Umfang: |
14 |
|---|
| 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.] |
|---|---|
| Übergeordnetes Werk: |
volume:297 ; year:2017 ; pages:36-49 ; extent:14 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.expneurol.2017.07.006 |
|---|
| Katalog-ID: |
ELV036170216 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV036170216 | ||
| 003 | DE-627 | ||
| 005 | 20230625211123.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2017 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.expneurol.2017.07.006 |2 doi | |
| 028 | 5 | 2 | |a GBVA2017020000027.pica |
| 035 | |a (DE-627)ELV036170216 | ||
| 035 | |a (ELSEVIER)S0014-4886(17)30180-2 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 630 |a 640 |q VZ |
| 084 | |a 48.30 |2 bkl | ||
| 100 | 1 | |a Jin, Na |e verfasserin |4 aut | |
| 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 |
| 264 | 1 | |c 2017transfer abstract | |
| 300 | |a 14 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 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 | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Xu, Chao ELSEVIER |t Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation |d 2022 |d a journal of neuroscience research |g Amsterdam [u.a.] |w (DE-627)ELV008416567 |
| 773 | 1 | 8 | |g volume:297 |g year:2017 |g pages:36-49 |g extent:14 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.expneurol.2017.07.006 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 936 | b | k | |a 48.30 |j Natürliche Ressourcen |x Land- und Forstwirtschaft |q VZ |
| 951 | |a AR | ||
| 952 | |d 297 |j 2017 |h 36-49 |g 14 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
n j nj |
|---|---|
| matchkey_str |
jinnazhuhuazhangliangxiaohuangweixieqing:2017----:oimeeaeciaewtaeisgaignrpesdmlifrainntiltase |
| hierarchy_sort_str |
2017transfer abstract |
| bklnumber |
48.30 |
| publishDate |
2017 |
| allfields |
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 |
| spelling |
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 |
| language |
English |
| source |
Enthalten in Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation Amsterdam [u.a.] volume:297 year:2017 pages:36-49 extent:14 |
| sourceStr |
Enthalten in Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation Amsterdam [u.a.] volume:297 year:2017 pages:36-49 extent:14 |
| format_phy_str_mv |
Article |
| bklname |
Natürliche Ressourcen |
| institution |
findex.gbv.de |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation |
| authorswithroles_txt_mv |
Jin, Na @@aut@@ Zhu, Huazhang @@oth@@ Liang, Xiao @@oth@@ Huang, Wei @@oth@@ Xie, Qingguo @@oth@@ Xiao, Peng @@oth@@ Ni, Jiazuan @@oth@@ Liu, Qiong @@oth@@ |
| publishDateDaySort_date |
2017-01-01T00:00:00Z |
| hierarchy_top_id |
ELV008416567 |
| dewey-sort |
3610 |
| id |
ELV036170216 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV036170216</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625211123.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.expneurol.2017.07.006</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2017020000027.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV036170216</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-4886(17)30180-2</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">630</subfield><subfield code="a">640</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">48.30</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Jin, Na</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">14</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhu, Huazhang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liang, Xiao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Huang, Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xie, Qingguo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xiao, Peng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ni, Jiazuan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Qiong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Xu, Chao ELSEVIER</subfield><subfield code="t">Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation</subfield><subfield code="d">2022</subfield><subfield code="d">a journal of neuroscience research</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV008416567</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:297</subfield><subfield code="g">year:2017</subfield><subfield code="g">pages:36-49</subfield><subfield code="g">extent:14</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.expneurol.2017.07.006</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">48.30</subfield><subfield code="j">Natürliche Ressourcen</subfield><subfield code="x">Land- und Forstwirtschaft</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">297</subfield><subfield code="j">2017</subfield><subfield code="h">36-49</subfield><subfield code="g">14</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Jin, Na |
| spellingShingle |
Jin, Na ddc 610 ddc 630 bkl 48.30 Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
| authorStr |
Jin, Na |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV008416567 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 630 - Agriculture & related technologies 640 - Home & family management |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 630 640 VZ 48.30 bkl Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
| topic |
ddc 610 ddc 630 bkl 48.30 |
| topic_unstemmed |
ddc 610 ddc 630 bkl 48.30 |
| topic_browse |
ddc 610 ddc 630 bkl 48.30 |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
h z hz x l xl w h wh q x qx p x px j n jn q l ql |
| hierarchy_parent_title |
Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation |
| hierarchy_parent_id |
ELV008416567 |
| dewey-tens |
610 - Medicine & health 630 - Agriculture 640 - Home & family management |
| hierarchy_top_title |
Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV008416567 |
| title |
Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
| ctrlnum |
(DE-627)ELV036170216 (ELSEVIER)S0014-4886(17)30180-2 |
| title_full |
Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
| author_sort |
Jin, Na |
| journal |
Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation |
| journalStr |
Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2017 |
| contenttype_str_mv |
zzz |
| container_start_page |
36 |
| author_browse |
Jin, Na |
| container_volume |
297 |
| physical |
14 |
| class |
610 610 DE-600 630 640 VZ 48.30 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Jin, Na |
| doi_str_mv |
10.1016/j.expneurol.2017.07.006 |
| dewey-full |
610 630 640 |
| title_sort |
sodium selenate activated wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of alzheimer's disease |
| title_auth |
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. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
| title_short |
Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease |
| url |
https://doi.org/10.1016/j.expneurol.2017.07.006 |
| remote_bool |
true |
| author2 |
Zhu, Huazhang Liang, Xiao Huang, Wei Xie, Qingguo Xiao, Peng Ni, Jiazuan Liu, Qiong |
| author2Str |
Zhu, Huazhang Liang, Xiao Huang, Wei Xie, Qingguo Xiao, Peng Ni, Jiazuan Liu, Qiong |
| ppnlink |
ELV008416567 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.expneurol.2017.07.006 |
| up_date |
2024-07-06T19:29:44.375Z |
| _version_ |
1803859194675200000 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV036170216</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625211123.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.expneurol.2017.07.006</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2017020000027.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV036170216</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-4886(17)30180-2</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">630</subfield><subfield code="a">640</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">48.30</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Jin, Na</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">14</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhu, Huazhang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liang, Xiao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Huang, Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xie, Qingguo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xiao, Peng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ni, Jiazuan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Qiong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Xu, Chao ELSEVIER</subfield><subfield code="t">Identification of lignocellulosic derivatives inhibiting succinic acid fermentation and molecular mechanism investigation</subfield><subfield code="d">2022</subfield><subfield code="d">a journal of neuroscience research</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV008416567</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:297</subfield><subfield code="g">year:2017</subfield><subfield code="g">pages:36-49</subfield><subfield code="g">extent:14</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.expneurol.2017.07.006</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">48.30</subfield><subfield code="j">Natürliche Ressourcen</subfield><subfield code="x">Land- und Forstwirtschaft</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">297</subfield><subfield code="j">2017</subfield><subfield code="h">36-49</subfield><subfield code="g">14</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.400222 |