| dc.description.abstract | In this study, BDNF, a neurotrophin family member, was selected as the target molecule of TTP and hsa-miR-16 genes using bioinformatics methods.
Methods: BDNF was identified as the target gene for TTP and ROQUIN from the AU-rich elements database. Through the miRTarBase and miRWalk databases, which provide valid miRNAs, miR-16 was selected as a miRNA that targets the BDNF target gene. The Gene Expression Omnibus database included two microarray datasets, including information on mRNAs (GSE106241) and miRNAs (GSE157239) from individuals with AD, and corresponding controls were downloaded. R software was used to identify mRNAs and miRNAs with different expressions. Among the results, the expression of the desired genes was measured together, and diagrams of expression correlation were drawn in the brain tissue of patients compared to the brain tissue of healthy controls. Q-PCR was also used to evaluate the expression of these regulatory factors on the expression of the BDNF target gene in the blood of 50 AD and 50 control patients.
Results: Bioinformatics evaluation showed that TTP acts as a post-transcriptional regulatory factor to control BDNF expression in AD disease in temporomandibular cortex (TC) tissue samples by increasing expression. Instead, this expression pattern was not found in peripheral blood samples from people with AD and normal controls. On the other hand, ROQUIN expression was increased in the peripheral blood of AD patients. Hsa-miR-16-5p levels did not show significant differences in peripheral blood samples. Finally, it was shown that TTP and hsa-miR-16-5p, based on the evaluation of the receiver operating characteristic (ROC), effectively identify AD patients from healthy controls. | en_US |
