scholarly journals Differentially expressed genes in Alzheimer’s disease highlighting the roles of microglia genes including OLR1 and astrocyte gene CDK2AP1

2021 ◽  
Vol 13 ◽  
pp. 100227 ◽  
Author(s):  
Qingqin S. Li ◽  
Louis De Muynck
Hereditas ◽  
2021 ◽  
Vol 158 (1) ◽  
Author(s):  
Haoming Li ◽  
Linqing Zou ◽  
Jinhong Shi ◽  
Xiao Han

Abstract Background Alzheimer’s disease (AD) is a fatal neurodegenerative disorder, and the lesions originate in the entorhinal cortex (EC) and hippocampus (HIP) at the early stage of AD progression. Gaining insight into the molecular mechanisms underlying AD is critical for the diagnosis and treatment of this disorder. Recent discoveries have uncovered the essential roles of microRNAs (miRNAs) in aging and have identified the potential of miRNAs serving as biomarkers in AD diagnosis. Methods We sought to apply bioinformatics tools to investigate microarray profiles and characterize differentially expressed genes (DEGs) in both EC and HIP and identify specific candidate genes and pathways that might be implicated in AD for further analysis. Furthermore, we considered that DEGs might be dysregulated by miRNAs. Therefore, we investigated patients with AD and healthy controls by studying the gene profiling of their brain and blood samples to identify AD-related DEGs, differentially expressed miRNAs (DEmiRNAs), along with gene ontology (GO) analysis, KEGG pathway analysis, and construction of an AD-specific miRNA–mRNA interaction network. Results Our analysis identified 10 key hub genes in the EC and HIP of patients with AD, and these hub genes were focused on energy metabolism, suggesting that metabolic dyshomeostasis contributed to the progression of the early AD pathology. Moreover, after the construction of an miRNA–mRNA network, we identified 9 blood-related DEmiRNAs, which regulated 10 target genes in the KEGG pathway. Conclusions Our findings indicated these DEmiRNAs having the potential to act as diagnostic biomarkers at an early stage of AD.


2006 ◽  
Vol 14 (7S_Part_27) ◽  
pp. P1452-P1452
Author(s):  
Xue Wang ◽  
Mariet Allen ◽  
Minerva M. Carrasquillo ◽  
Jeremy D. Burgess ◽  
Shaoyu Li ◽  
...  

2018 ◽  
Vol 17 (8) ◽  
pp. 608-617 ◽  
Author(s):  
Xiao-wen Jiang ◽  
Hong-yuan Lu ◽  
Ziru Xu ◽  
Tian-yi Liu ◽  
Qiong Wu ◽  
...  

Background: Epilepsy and Alzheimer's disease are common neuropathies with a complex pathogenesis. Both of them have some correlations in etiology, pathogenesis, pathological changes, clinical manifestations and treatment. Objective: This study investigated the key genes and molecular genetic mechanism in epilepsy and Alzheimer’s disease by bioinformatics analysis. Method: Two gene expression profiles were used to screen differentially expressed genes by GEO2R tool. The Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway enrichment analysis was performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID). Then the protein-protein interaction (PPI) network was constructed by Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape software which can be used to analyze modules with MCODE. Results: A total of 199 differentially expressed genes (DEGs) in the two groups. According to GO_BP analysis and KEGG pathway enrichment by DAVID, we found DEGs referring to several pathways significantly down-regulated in endocytosis, such as endocytosis, synaptic vesicle cycle, lysosome, cAMP signaling pathway, circadian entrainment, LTP, glutamatergic synapse and GABAergic synapse pathway. The regulator genes of the upstream pathway of circadian rhythms were obviously downgraded. Conclusion: Our research demonstrated that the regulatory genes of the upstream pathway of circadian rhythms were obviously downgraded. These biological pathways and DEGs or hub genes may contribute to revealing the molecular relationship between Alzheimer's disease and epilepsy.


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