|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
Mechanistically, VPA treatment increased β-catenin levels, accumulated the inactive form of glycogen synthase kinase-3β (GSK-3β), and induced the expression of NeuroD1, a Wnt target gene involved in neurogenesis, suggesting the activation of the Wnt signaling pathway in the hippocampus of 3xTgAD mice.
|
30971911 |
2019 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Correction to: Neuroprotective Role of Novel Triazine Derivatives by Activating Wnt/β Catenin Signaling Pathway in Rodent Models of Alzheimer's Disease.
|
31463875 |
2019 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Combining bioinformatics with RNA and protein analysis, we identified downregulation of the Wnt/β-catenin pathway in the hippocampus of adult DS individuals with Alzheimer's disease and the 'Tc1' DS mouse model.
|
31086297 |
2019 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
In the brain, dysfunctions in Wnt signalling related to beta-catenin levels may also cause various pathological conditions like Alzheimer's disease, Parkinson's disease, and depression.
|
29490303 |
2019 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, we demonstrated that Akt/Wnt/β-catenin pathway protein expression in the hippocampus was suppressed in a mouse model of AD and TGF-β1 significantly enhanced the phosphorylation Akt, GSK3β, and increased the nuclear β-catenin.
|
30539409 |
2019 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
In this study, we provide evidence that rapamycin inhibits GSK3β activation and elevates β‑catenin expression by improving the Wnt3a expression levels, which facilitates the amelioration of AD pathology.
|
31115485 |
2019 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
The present review focusses on the thermodynamic implications in the reprogramming of cellular energy metabolism enabling in Alzheimer's disease (AD) through the opposite interplay of the molecular signaling pathways WNT/β-catenin and PPARγ.
|
29079469 |
2018 |
|
Alzheimer's Disease
|
0.300 |
GeneticVariation
|
disease |
BEFREE |
Evidence of Wnt/β-catenin alterations in brain and bone of a tauopathy mouse model of Alzheimer's disease.
|
29660685 |
2018 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, a reduction in the levels of nuclear β-catenin was detected in AD brains compared to controls as well as a decrease in the expression of the inactive phosphorylated Glycogen synthase kinase 3 (GSK3) isoform.
|
30176342 |
2018 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
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.
|
28711506 |
2017 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
Downregulation of Wnt/β-catenin, through activation of glycogen synthase kinase-3β (GSK-3β) by Aβ, and inactivation of phosphatidylinositol 3-kinase/Akt signaling involve oxidative stress in AD.
|
28981597 |
2017 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
In consequence, β-catenin and GSK3 are targets for potential treatments in AD.
|
28635355 |
2017 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Presenilins are the enzymatic components of γ-secretase complex that cleaves amyloid precursor protein, Notch and β-catenin, which has critical roles in the development of Alzheimer's disease and cancer cell growth.
|
24858037 |
2014 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
The protein levels of KLF8 and β-catenin were increased, while the level of NF-κB was decreased in the AD model.
|
24114572 |
2014 |
|
Alzheimer's Disease
|
0.300 |
GeneticVariation
|
disease |
BEFREE |
We now report that miR-342-5p is upregulated in APP/PS1, PS1ΔE9, and PS1-M146V transgenic AD mice, and that this upregulation is mechanistically linked to elevated β-catenin, c-Myc, and interferon regulatory factor-9.
|
24440716 |
2014 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
Importantly, our results further showed that HupA inhibited GSK3α/β activity, and enhanced the β-catenin level in the transgenic mouse brain and in SH-SY5Y cells overexpressing Swedish mutation APP, suggesting that the neuroprotective effect of HupA is not related simply to its AChE inhibition and antioxidation, but also involves other mechanisms, including targeting of the Wnt/β-catenin signaling pathway in AD brain.
|
21289607 |
2011 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
Here, we report increased β-catenin expression, a central intracellular component of WNT signaling, in microglia undergoing a proinflammatory morphogenic transformation under pathogenic conditions associated with neuroinflammation such as Alzheimer's disease.
|
20967887 |
2011 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
The study aims to investigate the effect of Curcumin on the expression of GSK-3β, β-catenin and CyclinD1 in vitro, which are tightly correlated with Wnt/β-catenin signaling pathway, and also to explore the mechanisms, which will provide a novel therapeutic intervention for treatment of Alzheimer's disease.
|
21352912 |
2011 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Analysis of the microarray expression data by Gene ontology (GO) and Gene Set Enrichment Analysis (GSEA) as well as significant pathway analysis by GeneSpring GX10 and Panther Classification System reveal that HPRT deficiency is accompanied by aberrations in a variety of pathways known to regulate neurogenesis or to be implicated in neurodegenerative disease, including the canonical Wnt/β-catenin and the Alzheimer's disease/presenilin signaling pathways.
|
21305049 |
2011 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Blocking IL-1 signaling rescues cognition, attenuates tau pathology, and restores neuronal β-catenin pathway function in an Alzheimer's disease model.
|
22095718 |
2011 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Here, we show that phosphorylation of CRMP2, CRMP4, β-catenin, c-Myc, c-Jun and some residues on tau associated with Alzheimer's disease, is altered in cortical tissue lacking both isoforms of GSK3.
|
20831597 |
2010 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Protocadherin 11X (Pcdh11X) has been suspected to be associated with Alzheimer's disease through participating in the metabolism of PP1α and β-catenin or by altering the synaptic functions.
|
20707987 |
2010 |
|
Alzheimer's Disease
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
We report here that: (a) a bioinformatic analysis of 15,476 promoters of the human genome predicted several Wnt target genes, being CaMKIV a very interesting candidate; (b) CaMKIV promoter contains TCF/LEF transcription motifs similar to those present in Wnt target genes; (c) biochemical studies indicate that lithium and the canonical ligand Wnt-3a induce CaMKIV mRNA and protein expression levels in rat hippocampal neurons as well as CaMKIV promoter activity; (d) treatment of hippocampal neurons with Wnt-3a increases the binding of beta-catenin to the CaMKIV promoter: (e) In vivo activation of the Wnt signaling improve spatial memory impairment and restores the expression of CaMKIV in a mice double transgenic model for Alzheimer's disease which shows decreased levels of the kinase.
|
19711354 |
2009 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Since Abeta(1-42)-induced TGF-beta1, we suggest that TGF-beta1 may amplify Abeta(1-42)-mediated neurodegeneration in AD via Smad7 and beta-catenin interaction and nuclear localization.
|
18063474 |
2008 |
|
Alzheimer's Disease
|
0.300 |
Biomarker
|
disease |
BEFREE |
Therefore, the overexpression of NSE/htau23 in the brains of transgenic mice induces abnormal phosphorylations of tau, GSK3beta, and beta-catenin, which are ultimately linked to neuronal degeneration in cases of AD.
|
17337327 |
2007 |