Amyloid protein-mediated differential DNA methylation status regulates gene expression in Alzheimer’s disease model cell line

2011 ◽  
Vol 414 (4) ◽  
pp. 700-705 ◽  
Author(s):  
Hye Youn Sung ◽  
Eun Nam Choi ◽  
Sangmee Ahn Jo ◽  
Seikwan Oh ◽  
Jung-Hyuck Ahn
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Methylation ◽  
Cell Line ◽  
Methylation Status ◽  
Disease Model ◽  
Amyloid Protein ◽  
Model Cell

Amyloid-β Alters the DNA Methylation Status of Cell-fate Genes in an Alzheimer's Disease Model

2013 ◽  
Vol 38 (4) ◽  
pp. 831-844 ◽  
Author(s):  
Noor Taher ◽  
Courtney McKenzie ◽  
Rebecca Garrett ◽  
Matthew Baker ◽  
Nena Fox ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Methylation ◽  
Cell Fate ◽  
Methylation Status ◽  
Disease Model ◽  
Amyloid Β

Effect of Gene Editing on Alzheimer's Disease

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Noha nageh mohamed ◽  
Maha mohammed sallam ◽  
Marwa Ali Abd El-Khalek ◽  
Mohamed Mahmoud Fouad
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Viability ◽  
Cell Line ◽  
Cause Of Death ◽  
Gene Editing ◽  
The United States ◽  
Amyloid Protein ◽  
App Gene

Abstract Background Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and, eventually, the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Current estimates suggest that 44 million people live with dementia worldwide at present. This is predicted to more than triple by 2050 as the population ages. Alzheimer’s disease is currently ranked as the sixth leading cause of death in the United States, but recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people Treatment is currently targeted toward symptomatic therapy, although trials are underway that aim to reduce the production and overall burden of pathology within the brain. Recently, the Clustered Regular Interspaced Short Palindromic Repeats (CRISPR-cas9) has shown promise in certain neurological disorders, it provides a precise editing to human genome and reflect an efficient curative therapy. We aimed to investigate the efficacy of knock-out of the APP gene “Amyloid precursor protein gene(APBA2)that consequently modify the expression of Amyloid protein in leucocytes cell line using CRISPR-cas9 technology. Methods The gene expression profile of Alzheimer's disease was downloaded from biological bioinformatics databases,and based on bioinformatics analysis, we figured out that APP gene was overexpressed in Alzheimer's disease in both brain and peripheral tissues such as plasma, fibroblast and PMNLs. We used PMNLs as the source of gene for edition in our study .We knocked out the APP gene in leucocytes cell lines using CRISPR-cas9 technology. Finally, the gene editing efficacy was evaluated by cell viability assay, the gene expression was measured by qPCR and the Amyloid protein expression was proved by Immunofluorescence. Results knockout of APP gene int Leucocytes Cell line resulted in reduction in cell viability that was associated with marked reduction in the amyloid protein and gene expressions. Conclusion knockout of APP(APBA2) gene represents a promising therapeutic strategy in Alzheimer's disease.

scholarly journals Integrated DNA methylation and gene expression profiling across multiple brain regions implicate novel genes in Alzheimer’s disease

2019 ◽  
Vol 137 (4) ◽  
pp. 557-569 ◽  
Author(s):  
Stephen A. Semick ◽  
Rahul A. Bharadwaj ◽  
Leonardo Collado-Torres ◽  
Ran Tao ◽  
Joo Heon Shin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Methylation ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Brain Regions ◽  
Novel Genes

O3-04-06: GENE EXPRESSION PROFILING AND DNA METHYLATION IN ALZHEIMER'S DISEASE BRAINS

2014 ◽  
Vol 10 ◽  
pp. P216-P216
Author(s):  
Mariet Allen ◽  
Daniel Serie ◽  
Zhifu Sun ◽  
Saurabh Baheti ◽  
Mike Walsh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Methylation ◽  
Gene Expression Profiling ◽  
Expression Profiling

scholarly journals Nutrigenomic Studies on the Ameliorative Effect of Enzyme-Digested Phycocyanin in Alzheimer’s Disease Model Mice

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4431
Author(s):  
Yasuyuki Imai ◽  
Yurino Koseki ◽  
Makoto Hirano ◽  
Shin Nakamura
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Oral Administration ◽  
Expression Patterns ◽  
Disease Model ◽  
Neuroprotective Effects ◽  
Aberrant Expression ◽  
Ameliorative Effect

Alzheimer’s disease (AD) is the most common form of dementia, and the cognitive impairments associated with this degenerative disease seriously affect daily life. Nutraceuticals for the prevention or delay of AD are urgently needed. It has been increasingly observed that phycocyanin (PC) exerts neuroprotective effects. AD model mice intracerebroventricularly injected with amyloid beta-peptide 25–35 (Aβ25–35) at 10 nmol/head displayed significant cognitive impairment in the spontaneous alternation test. Cognitive impairment was significantly ameliorated in mice treated with 750 mg/kg of enzyme-digested (ED) PC by daily oral administration for 22 consecutive days. Application of DNA microarray data on hippocampal gene expression to nutrigenomics studies revealed that oral EDPC counteracted the aberrant expression of 35 genes, including Prnp, Cct4, Vegfd (Figf), Map9 (Mtap9), Pik3cg, Zfand5, Endog, and Hbq1a. These results suggest that oral administration of EDPC ameliorated cognitive impairment in AD model mice by maintaining and/or restoring normal gene expression patterns in the hippocampus.

scholarly journals Integrated DNA methylation and gene expression profiling across multiple brain regions implicate novel genes in Alzheimer’s disease

2018 ◽  
Author(s):  
Stephen A. Semick ◽  
Rahul A. Bharadwaj ◽  
Leonardo Collado-Torres ◽  
Ran Tao ◽  
Joo Heon Shin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Methylation ◽  
Neurodegenerative Disorder ◽  
Late Onset ◽  
Brain Regions ◽  
Epigenetic Mechanism ◽  
Novel Genes ◽  
Age Related

AbstractBackgroundLate-onset Alzheimer’s disease (AD) is a complex age-related neurodegenerative disorder that likely involves epigenetic factors. To better understand the epigenetic state associated with AD represented as variation in DNA methylation (DNAm), we surveyed 420,852 DNAm sites from neurotypical controls (N=49) and late-onset AD patients (N=24) across four brain regions (hippocampus, entorhinal cortex, dorsolateral prefrontal cortex and cerebellum).ResultsWe identified 858 sites with robust differential methylation, collectively annotated to 772 possible genes (FDR<5%, within 10kb). These sites were overrepresented in AD genetic risk loci (p=0.00655), and nearby genes were enriched for processes related to cell-adhesion, immunity, and calcium homeostasis (FDR<5%). We analyzed corresponding RNA-seq data to prioritize 130 genes within 10kb of the differentially methylated sites, which were differentially expressed and had expression levels associated with nearby DNAm levels (p<0.05). This validated gene set includes previously reported (e.g. ANK1, DUSP22) and novel genes involved in Alzheimer’s disease, such as ANKRD30B.ConclusionsThese results highlight DNAm changes in Alzheimer’s disease that have gene expression correlates, implicating DNAm as an epigenetic mechanism underlying pathological molecular changes associated with AD. Furthermore, our framework illustrates the value of integrating epigenetic and transcriptomic data for understanding complex disease.

Angiotensin II triggers autophagy and apoptosis in PC12 cell line: An in vitro Alzheimer’s disease model

2019 ◽  
Vol 1718 ◽  
pp. 46-52 ◽  
Author(s):  
Minjie Tian ◽  
Xingjian Lin ◽  
Liang Wu ◽  
Jie Lu ◽  
Yingdong Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Ii ◽  
Cell Line ◽  
Pc12 Cell ◽  
Disease Model ◽  
Pc12 Cell Line
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