Evaluation of SNPs and miRNAs in the BID, MAPK10, and AGER Genes Related to Alzheimer's Disease by Using In Silico Tools

Abstract

Alzheimer's disease (AD) is a multifactorial disease resulting from both genetic and environmental factors, which are pathologically defined by the accumulation of intracellular hyperphosphorylated tau protein, neurofibrils tangles, and extracellular amyloid β protein in the brain. The purpose of this study is to estimate the potentially damaging effects of missense single nucleotide polymorphisms (SNPs) in the BID, MAPK10 and AGER genes associated with AD using various in silico tools and to determine the effects of SNPs on miRNAs. In addition, it is aimed to determine the gene-gene and protein-protein interactions through various software tools. Consequently, it was estimated that there may be harmful effects of seven polymorphisms in the BID gene, twenty-seven in the MAPK10 gene and three in the AGER gene. It was obtained that some SNPs decrease the effectiveness of miRNA-mRNA binding, enhance, break, create a new binding zone and/or destroy the miRNA-mRNA binding zone in the BID and MAPK10 genes. miRNA-SNP analyses could not provide information on the AGER gene. In this study, SNPs in the BID, MAPK10, and AGER genes, which are estimated to be high-risk SNPs, will be able to provide data for future genotyping studies. SNPs that are estimated to be high-risk and SNPs that may have a role in miRNA- mRNA activity can be assessed as a priority in experimental studies related to AD. In the future, experimental studies are proposed to investigate the clinical effects of harmful/disease-related missense SNPs and SNPs affecting mRNA-miRNA interaction.