Comprehensive Analysis of Differential Expression Profiles of Long Non-coding RNAs with Associated Co-expression and Competing Endogenous RNA Networks in the Hippocampus of Patients with Alzheimer's Disease

2021 ◽  
Vol 18 ◽  
Author(s):  
Jian-Jun Zhang ◽  
Ze-Xuan-Zhu ◽  
Guang-Min-Xu ◽  
Peng Su ◽  
Qian Lei ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Expression Profiles ◽  
Gene Expression Omnibus ◽  
Competing Endogenous Rna ◽  
Pathogenic Genes ◽  
Non Coding Rna ◽  
Using Data ◽  
Trans Regulation

Background: Alzheimer's disease (AD) is still one of the major threats to human health. Although a satisfactory treatment for AD has not yet been discovered, it is necessary to continue to search for novel approaches to deal with this insidious and debilitating disease. Although numerous studies have shown that long non-coding RNA (lncRNA) occupy a significant role in a variety of diseases, their roles in AD remain unclear. Objectives: Using data analysis to explore the role of lncRNA in the course of AD, to further our understanding of AD, and to look forward to finding a new breakthrough for the treatment of AD. Methods: We downloaded and screened expression data of the hippocampal regions of patients with AD from the Gene Expression Omnibus database. We generated lncRNA-miRNA-mRNA networks based on the competing endogenous RNA (ceRNA) hypothesis, and according to gene expression level, we constructed a coding-noncoding co-expression (CNC) network and then executed cis- and trans-regulation analyses. Results: Through comprehensive and systematic analyses, we found that lncRNAs MALAT1, OIP5-AS1, LINC00657, and lnc-NUMB-1 regulated the expression of the key AD pathogenic genes APP, PSEN1, BACE1; and that these lncRNAs may promote the distribution of β-amyloid (Aβ protein) in the brain through exosomes. In addition, lncRNAs were found to adjust viral transcriptional expression, thereby further supporting viral pathogenesis for AD. Conclusions: The lncRNAs MALAT1, OIP5-AS1, LINC00657, and lnc-NUMB-1 that are present in the hippocampus of AD patients exert an important influence on the development of this disease.

Gene expression profiles of metabolic enzyme transcripts in Alzheimer's disease

2007 ◽  
Vol 1127 ◽  
pp. 127-135 ◽  
Author(s):  
Wendy M. Brooks ◽  
Patrick J. Lynch ◽  
Catherine C. Ingle ◽  
Alexander Hatton ◽  
Piers C. Emson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Metabolic Enzyme

Gene Expression Profiles of Entorhinal Cortex in Alzheimer’s Disease

2014 ◽  
Vol 29 (6) ◽  
pp. 526-532 ◽  
Author(s):  
Bingqian Ding ◽  
Yan Xi ◽  
Ming Gao ◽  
Zhenjiang Li ◽  
Chenyang Xu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Entorhinal Cortex ◽  
Expression Profiles ◽  
Gene Expression Profiles

scholarly journals Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set

2008 ◽  
Vol 33 (2) ◽  
pp. 240-256 ◽  
Author(s):  
Winnie S. Liang ◽  
Travis Dunckley ◽  
Thomas G. Beach ◽  
Andrew Grover ◽  
Diego Mastroeni ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Expression Profiles ◽  
Brain Regions ◽  
Elderly Persons ◽  
Data Set ◽  
Healthy Elderly ◽  
Neuronal Gene ◽  
Laser Capture

Alzheimer's Disease (AD) is the most widespread form of dementia during the later stages of life. If improved therapeutics are not developed, the prevalence of AD will drastically increase in the coming years as the world's population ages. By identifying differences in neuronal gene expression profiles between healthy elderly persons and individuals diagnosed with AD, we may be able to better understand the molecular mechanisms that drive AD pathogenesis, including the formation of amyloid plaques and neurofibrillary tangles. In this study, we expression profiled histopathologically normal cortical neurons collected with laser capture microdissection (LCM) from six anatomically and functionally discrete postmortem brain regions in 34 AD-afflicted individuals, using Affymetrix Human Genome U133 Plus 2.0 microarrays. These regions include the entorhinal cortex, hippocampus, middle temporal gyrus, posterior cingulate cortex, superior frontal gyrus, and primary visual cortex. This study is predicated on previous parallel research on the postmortem brains of the same six regions in 14 healthy elderly individuals, for which LCM neurons were similarly processed for expression analysis. We identified significant regional differential expression in AD brains compared with control brains including expression changes of genes previously implicated in AD pathogenesis, particularly with regard to tangle and plaque formation. Pinpointing the expression of factors that may play a role in AD pathogenesis provides a foundation for future identification of new targets for improved AD therapeutics. We provide this carefully phenotyped, laser capture microdissected intraindividual brain region expression data set to the community as a public resource.

scholarly journals Supervised pathway analysis of blood gene expression profiles in Alzheimer's disease

2019 ◽  
Vol 84 ◽  
pp. 98-108 ◽  
Author(s):  
Elaheh Moradi ◽  
Mikael Marttinen ◽  
Tomi Häkkinen ◽  
Mikko Hiltunen ◽  
Matti Nykter
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pathway Analysis ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Blood Gene Expression

scholarly journals The middle temporal gyrus is transcriptionally altered in patients with Alzheimer’s Disease.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcriptional Repression ◽  
Zinc Finger Protein ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Global Gene Expression ◽  
Middle Temporal Gyrus ◽  
Middle Temporal

We sought to understand, at the systems level and in an unbiased fashion, how gene expression was most different in the brains of patients with Alzheimer’s Disease (AD) by mining published microarray datasets (1, 2). Comparing global gene expression profiles between patient and control revealed that a set of 84 genes were expressed at significantly different levels in the middle temporal gyrus (MTG) of patients with Alzheimer’s Disease (1, 2). We used computational analyses to classify these genes into known pathways and existing gene sets, and to describe the major differences in the epigenetic marks at the genomic loci of these genes. While a portion of these genes is computationally cognizable as part of a set of genes up-regulated in the brains of patients with AD (3), many other genes in the gene set identified here have not previously been studied in association with AD. Transcriptional repression, both pre- and post-transcription appears to be affected; nearly 40% of these genes are transcriptional targets of MicroRNA-19A/B (miR-19A/B), the zinc finger protein 10 (ZNF10), or of the AP-1 repressor jun dimerization protein 2 (JDP2).

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