Abstract
Alzheimer's disease (AD), the most frequently diagnosed dementia, is a senile neurodegenerative disorder characterized by amnesia and cognitive dysfunction. Unfortunately, there are still no successful strategies to prevent AD progression. Thus, the vast majority of research focuses on recognizing risk factors for developing and progressing this disease. Human spirochetes, fungi, Borrelia burgdorferi, Chlamydophila pneumoniae, Helicobacter pylori, and human herpes simplex virus type 1 (HSV-1) have all been implicated in the development and progression of AD. Identifying microRNAs (miRs) encoded by DNA viruses has indicated that viruses can be evolved to exploit RNA silencing to regulate host and viral genes. Similar to host miR, v-miR can interact with the 3' untranslated region (UTR) of the target mRNA to regulate gene expression. Although HSV-1 can also encode various miRs, their significance in the development and progression of AD is still unclear. In the present study, utilizing the bioinformatics approach (R software and related packages), we analyzed the differentially expressed genes (DEGs) in AD samples (grey matter) of GSE37263 dataset obtained from the NCBI Gene Expression Omnibus (GEO). Then, the sequences of HSV-1-encoded-miRs were retrieved from miRbase, and their targets were predicted by miRDB. Afterward, the common genes between downregulated DEGs in AD and targets of HSV-1-encoded miRs were identified to shed new light on the relationship between HSV-1 infection and AD development. Our results have indicated that HSV-1-encoded-miRs can target the downregulated DEGs in AD, and these aberrant interactions can offer valuable diagnostic/prognostic biomarkers for affected patients.