Introduction: Alzheimer's disease (AD) is a neurodegenerative disorder that is primarily characterized by progressive cognitive decline and memory impairment. Caenorhabditis elegans (C. elegans), a nematode worm, is a valuable model organism because of its simplicity, genetic traceability, and well-mapped nervous system.

Methods: This study employs a systematic bioinformatics approach to identify and analyze conserved genes and pathways related to AD within the genomes of humans and C. elegans. Proteins altered in AD were obtained from NeuroPro (https://neuropro.biomedical.hosting/), including 4743 proteins.

Results: A total of 1642 genes in C. elegans orthologous to the most dysregulated AD-related genes in humans were identified, and the GO terms and pathways were compared to study the conserved pathways between the two species. A PPI network of dysregulated genes was constructed to infer the functions of AD-related orthologous genes in C. elegans. Orthologous gene protein–protein interaction (PPI) network analysis for dysregulated first neighbor genes reveals the hubs and important key regulators in C. elegans for upregulated genes are as follows: isw-1, enol-1, ruvb-2, tpi-1, eftu-2, ruvb-1, gpi-1, pgk-1, ubq-1, and let-716 for upregulated genes and rps-9, rps-18, rps-22, ubq-2, utx-1, T26E3.7, aco-2, rla-0, eef-1G, and tsfm-1 for downregulated genes.

Conclusion: Functional enrichment analysis and pathway mapping revealed the significant conservation of cellular mechanisms. Our findings highlight the utility of C. elegans as a model for AD, emphasizing the potential of bioinformatics in accentuating conserved biological processes and novel intervention strategies.