ISSN 2834-250X · Open Access · CC BY 4.0 For Authors Reviewers Contact

International Journal of Clinical & Medical Case Reports

ISSN 2834-250X · Case Reports · Clinical Images
International Journal of Clinical & Medical Case Reports
OPEN ACCESS

Investigation Of MiRNA-MiRNA Network And Critical Targets in The Progression Of Alzheimer’s Disease

Published: 29 Feb 2024 0 views

Abstract

Alzheimer’s disease (AD) is a neurologic ailment that causes the brain to atrophy and brain cells to die over time. AD is the most prevalent form of dementia, which is a gradual decrease in cognitive, behavioral, and social abilities that impairs a person’s capacity to operate independently. In this study, bioinformatics analysis was conducted to look into possible miRNA-mRNA couples implicated in the etiology of AD to find DEmiRNAs and genes unique to Alzheimer’s disease. Two suitable datasets (GSE18309 and GSE16759) from peripheral blood mononuclear cells (PBMCs) and the parietal lobe of AD patients were selected from the GEO database. Then, we used the online enrichment databases to evaluate signaling pathways, gene ontology, protein networks, and hub miRNAs. We Also used Cytoscape to design the interactive networks. Our results showed that, hsa-mir-765, hsa-mir-575, hsa-mir-425 3p, hsa-mir-198, hsa-mir-602, hsa-mir-601, hsa-mir-454-3p, hsa-mir-558, hsa-mir-448, and hsa-mir-542-5p were prominent role in exacerbate of AD. It was discovered that an abundance of miRNA-mRNA interactions implicated in synaptic transmission, aberrant protein degradation, and apoptosis. Additionally, EGF, ESR1, DLG4, CTTN, WASL, FN1, JUN, CDKN2A, and PRKCA gene expression in Alzheimer’s disease patients was considerably reduced in PBMCs. This study adds to our knowledge of the hsa-mir-765, hsa-mir-575, hsa-mir-425 3p, and hsa-mir-198 that may underlie Alzheimer’s disease and identifies novel diagnostic and therapeutic targets for the disease.

The full text of this article is available as a PDF. Download the PDF →

HTML full-text + structured metadata for this article are being processed (legacy import).