Unveiling Shared Gene Regulatory Networks and Pathways in Bipolar Disorder and Alzheimer’s Disease: Identifying Novel Therapeutic Targets and Drug Candidates
Bioinformatics involves interpreting biological processes to extract information from biological data, particularly in the context of genomics. Research indicates that Alzheimer’s Disease and Bipolar Disorder share many biochemical and genetic traits. For this study, we gather datasets from the Gene Expression Omnibus (GEO) at NCBI. Here some fundamental steps such as pre-processing, filtering, and connecting genes were made possible using the R programming language. These analyses have successfully scrutinized numerous common DEGs, with the number of associated microarray datasets GSE81396, and GSE48350. In our research aims to identify shared differentially expressed genes (DEGs), protein-protein interaction (PPI) networks, hub genes, key gene mi-RNA interactions, and transcription factors(TF) from gene regulatory networks (GRNs). Additionally, we will conduct a functional analysis using gene ontology to pinpoint significant biological functions and signaling pathways relevant to therapeutic targets for Alzheimer’s Disease and Bipolar Disorder. This study also seeks to inform drug design by exploring gene regulatory networks, protein-protein interactions, and protein-chemical interaction, thereby aiding in the development of effective treatments.
Authors
- Mohammad Sarwar Hossain Mollah (ORCID: https://orcid.org/0009-0007-0503-3652)
- Touhid Bhuiyan (ORCID: https://orcid.org/0000-0002-6747-0846)
- Marianne Rooman (ORCID: https://orcid.org/0000-0002-3810-7802)
- Urmi Bose
- Bikash Kumar Paul (ORCID: https://orcid.org/0000-0002-4414-2751)
- Md. Mehedi Hassan
Institutions
- Daffodil International University (BD)
- Mawlana Bhashani Science and Technology University (BD)
Publication Details
- Published
- 2024-11-28
- DOI
- https://doi.org/10.1109/becithcon64160.2024.10962661
- Primary Topic
- Bioinformatics and Genomic Networks
- Type
- article
- Field-Weighted Citation Impact
- 0.00