Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss and abnormal α-synuclein aggregation. Circulating microRNAs (miRNAs) have emerged as promising biomarkers and potential modulators of PD-related molecular pathways. In this study, we investigated the expression levels of four candidate miRNAs—miR-15a-5p, miR-16-5p, miR-139-5p, and miR-34a-3p—in patients with PD compared with healthy controls. A total of 47 PD patients and 45 age- and sex-matched controls were enrolled. Plasma miRNA levels were quantified using standardized RNA extraction, cDNA synthesis, and qPCR protocols. We observed marked upregulation of miR-15a-5p and robust downregulation of both miR-139-5p and miR-34a-3p in PD patients, whereas miR-16-5p showed no significant difference between groups. Target gene prediction and functional enrichment analysis identified 432 unique genes, with enrichment in biological processes related to protein ubiquitination and catabolic pathways, and signaling cascades such as mTOR, PI3K-Akt, MAPK, and Hippo pathways, all of which are implicated in neurodegeneration. Elevated miR-15a-5p may contribute to pro-apoptotic mechanisms, while reduced miR-139-5p and miR-34a-3p expression may reflect impaired mitochondrial function, diminished neuroprotection, or compensatory regulatory responses. Together, these dysregulated circulating miRNAs provide novel insight into PD pathophysiology and highlight their potential as accessible, non-invasive biomarkers. Further longitudinal studies in larger and more diverse cohorts are warranted to validate their diagnostic and prognostic value and to explore their utility as therapeutic targets.

Childhood obesity is a complex pathology that triggers early vascular damage through endoplasmic reticulum (ER) stress and fibrinolytic imbalance; however, the role of the ATF6/PLAT regulatory axis in this process has not yet been fully elucidated. This study aims to investigate the molecular basis of vascular risk by determining the expression levels of these genes and the potential regulatory hsa-miR-340-5p in children with obesity. Gene expression analyses were performed using the RT-qPCR method on blood samples obtained from 55 children with obesity and 40 healthy controls, while in silico protein–protein interaction (PPI) networks were mapped using the STRING database. The findings revealed that ATF6 expression was significantly downregulated (p < 0.001) and PLAT expression was significantly upregulated (p = 0.005) in the obese group compared to controls. No significant difference was detected in hsa-miR-340-5p levels (p = 0.447). PPI analysis confirmed the strong functional clustering of ATF6 with metabolic stress pathways and PLAT with coagulation cascades. In conclusion, the suppression of ATF6 in obesity indicates the “exhaustion” of adaptive cellular defense mechanisms, while the upregulation of PLAT points to a compensatory response to the chronic prothrombotic environment. These molecular alterations demonstrate that vascular risk in childhood obesity begins at the transcriptomic level long before clinical symptoms emerge, highlighting the ATF6/PLAT axis as a potential biomarker for early risk assessment.