Transcription factor Sp1 dysregulation in Alzheimer's disease

2008 ◽  
Vol 86 (11) ◽  
pp. 2499-2504 ◽  
Author(s):  
Bruce A. Citron ◽  
John S. Dennis ◽  
Ross S. Zeitlin ◽  
Valentina Echeverria
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Transcription Factor Sp1

scholarly journals Aβ-Induced Repressor Element 1-Silencing Transcription Factor (REST) Gene Delivery Suppresses Activation of Microglia-Like BV-2 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Tongya Yu ◽  
Hui Quan ◽  
Yuzhen Xu ◽  
Yunxiao Dou ◽  
Feihong Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Cell Activation ◽  
Type I ◽  
Hairpin Rna ◽  
Cell Dysfunction ◽  
Repressor Element

Compelling evidence from basic molecular biology has demonstrated the crucial role of microglia in the pathogenesis of Alzheimer’s disease (AD). Microglia were believed to play a dual role in both promoting and inhibiting Alzheimer’s disease progression. It is of great significance to regulate the function of microglia and make them develop in a favorable way. In the present study, we investigated the function of repressor element 1-silencing transcription factor (REST) in Aβ1-42-induced BV-2 cell dysfunction. We concluded that Aβ1-42 could promote type I activation of BV-2 cells and induce cell proliferation, migration, and proinflammation cytokine TNF-α, IL-1β, and IL-6 expression. Meanwhile, REST was upregulated, and nuclear translocalization took place due to Aβ1-42 stimulation. When REST was knocked down by a specific short hairpin RNA (sh-RNA), BV-2 cell proliferation, migration, and proinflammation cytokine expression and secretion induced by Aβ1-42 were increased, demonstrating that REST may act as a repressor of microglia-like BV-2 cell activation.

scholarly journals Decreased MEF2A Expression Regulated by Its Enhancer Methylation Inhibits Autophagy and May Play an Important Role in the Progression of Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Hui Li ◽  
Feng Wang ◽  
Xuqi Guo ◽  
Yugang Jiang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Methylation Level ◽  
Life Quality ◽  
Enrichment Analysis ◽  
Amyloid Plaques ◽  
Sequencing Data ◽  
Single Cell Sequencing ◽  
Enhancer Factor

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by amyloid plaques and neurofibrillary tangles which significantly affects people’s life quality. Recently, AD has been found to be closely related to autophagy. The aim of this study was to identify autophagy-related genes associated with the pathogenesis of AD from multiple types of microarray and sequencing datasets using bioinformatics methods and to investigate their role in the pathogenesis of AD in order to identify novel strategies to prevent and treat AD. Our results showed that the autophagy-related genes were significantly downregulated in AD and correlated with the pathological progression. Furthermore, enrichment analysis showed that these autophagy-related genes were regulated by the transcription factor myocyte enhancer factor 2A (MEF2A), which had been confirmed using si-MEF2A. Moreover, the single-cell sequencing data suggested that MEF2A was highly expressed in microglia. Methylation microarray analysis showed that the methylation level of the enhancer region of MEF2A in AD was significantly increased. In conclusion, our results suggest that AD related to the increased methylation level of MEF2A enhancer reduces the expression of MEF2A and downregulates the expression of autophagy-related genes which are closely associated with AD pathogenesis, thereby inhibiting autophagy.

Ouabain activates transcription factor EB and exerts neuroprotection in models of Alzheimer's disease

2019 ◽  
Vol 95 ◽  
pp. 13-24 ◽  
Author(s):  
Ha-Lim Song ◽  
Atanas Vladimirov Demirev ◽  
Na-Young Kim ◽  
Dong-Hou Kim ◽  
Seung-Yong Yoon
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Transcription Factor Eb

P1-079: NOVEL ROLE OF THE DEPRESSION-ASSOCIATED GATA1 TRANSCRIPTION FACTOR IN ALZHEIMER'S DISEASE

2014 ◽  
Vol 10 ◽  
pp. P332-P332 ◽  
Author(s):  
Jun Wang ◽  
Wei Zhao ◽  
Daniel Freire ◽  
Lap Ho ◽  
Giulio Maria Pasinetti
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Gata1 Transcription Factor

scholarly journals A nexus of miR-1271, PAX4 and ALK/RYK influences the cytoskeletal architectures in Alzheimer’s Disease and Type 2 Diabetes

2021 ◽  
Author(s):  
Piyali Majumder ◽  
Kaushik Chanda ◽  
Debajyoti Das ◽  
Brijesh Kumar Singh ◽  
Partha Chakrabarti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Type 2 Diabetes ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Tyrosine Kinases ◽  
Small Gtpases ◽  
Micro Rna ◽  
The Common ◽  
First Time

Alzheimer’s Disease (AD) and Type 2 Diabetes (T2D) share a common hallmark of insulin resistance. Reportedly, two non-canonical Receptor Tyrosine Kinases (RTKs), ALK and RYK, both targets of the same micro RNA miR-1271, exhibit significant and consistent functional downregulation in post-mortem AD and T2D tissues. Incidentally, both have Grb2 as a common downstream adapter and NOX4 as a common ROS producing factor. Here we show that Grb2 and NOX4 play critical roles in reducing the severity of both the diseases. The study demonstrates that the abundance of Grb2 in degenerative conditions, in conjunction with NOX4, reverse cytoskeletal degradation by counterbalancing the network of small GTPases. PAX4, a transcription factor for both Grb2 and NOX4, emerges as the key link between the common pathways of AD and T2D. Downregulation of both ALK and RYK through miR-1271, elevates the PAX4 level by reducing its suppressor ARX via Wnt/b-Catenin signaling. For the first time, this study brings together RTKs beyond Insulin Receptor (IR) family, transcription factor PAX4 and both AD and T2D pathologies on a common regulatory platform.

scholarly journals Exploring the Serum Level of RE1 Silencing Transcription Factor in Alzheimer’s Disease

2021 ◽  
Author(s):  
Shashank Shekhar ◽  
Manjari Tripathi ◽  
A. B. Dey ◽  
Sharmistha Dey
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Serum Levels ◽  
P Value ◽  
Standard Curve ◽  
Resonance Unit ◽  
Significant Difference ◽  
Duration Of Disease ◽  
And Gender

Abstract Objective The aim of this study was to evaluate the serum RE1 silencing transcription factor (REST) level in Alzheimer’s disease (AD), mild cognitive impairment (MCI), and elderly controls by using surface plasmon resonance (SPR) technology. Materials and Methods In this case–control study of 133 subjects, 49 patients with AD, 49 patients with MCI, and 35 elderly controls were recruited. The REST protein concentrations were evaluated by SPR. The resonance unit for each sample was recorded and the concentration of serum REST of study group was derived from the standard curve. All the experiments were done in triplicates. Statistical analysis was done and p-value of < 0.05 was considered as statistically significant. Results A significant difference was observed in the Montreal Cognitive Assessment score, Hindi Mental State Examination scale (HMSE) score education, disease duration, and gender among the groups. A significant (p>0.0001) difference in the duration of disease between AD and MCI was observed. It was observed that the mean concentration of serum REST was not significantly (p = 0.266) different among the groups. Conclusion This study first time evaluated the serum levels of REST in AD, MCI and age-matched elderly controls. The rest levels were similar in all groups; however, it can provide a new direction to future blood-based biomarker studies of REST.

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