scholarly journals Analysis of transcription factor- and ncRNA-mediated potential pathogenic gene modules in Alzheimer’s disease

Aging ◽  
2019 ◽  
Vol 11 (16) ◽  
pp. 6109-6119 ◽  
Author(s):  
Cuihua Zou ◽  
Jie Wang ◽  
Xiaohua Huang ◽  
Chongdong Jian ◽  
Donghua Zou ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Gene Modules ◽  
Pathogenic Gene

scholarly journals Shared Blood Transcriptomic Signatures between Alzheimer’s Disease and Diabetes Mellitus

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 34
Author(s):  
Taesic Lee ◽  
Hyunju Lee
Keyword(s):  
Diabetes Mellitus ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Interactions ◽  
Expression Patterns ◽  
Protein Protein Interactions ◽  
Hub Genes ◽  
Gene Modules ◽  
Gene Regulatory ◽  
The Brain

Alzheimer’s disease (AD) and diabetes mellitus (DM) are known to have a shared molecular mechanism. We aimed to identify shared blood transcriptomic signatures between AD and DM. Blood expression datasets for each disease were combined and a co-expression network was used to construct modules consisting of genes with similar expression patterns. For each module, a gene regulatory network based on gene expression and protein-protein interactions was established to identify hub genes. We selected one module, where COPS4, PSMA6, GTF2B, GTF2F2, and SSB were identified as dysregulated transcription factors that were common between AD and DM. These five genes were also differentially co-expressed in disease-related tissues, such as the brain in AD and the pancreas in DM. Our study identified gene modules that were dysregulated in both AD and DM blood samples, which may contribute to reveal common pathophysiology between two diseases.

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.

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