Parkinson’s disease (PD) is a complex and commonly spread neurodegenerative disorder that origins an extensive series of motor and non-motor indications. It is affected by the decline of dopamine neurons in the substantia nigra. There are many biomarkers for Parkinson’s disease (PD), like imaging biomarkers, inflammatory biomarkers, clinical biomarkers including sleep behavior disorder and fast eye movement, and biofluid-based biomarkers like extracellular vesicles and α-synuclein protein. Since miRNAs are tough and freely observable in biofluids, they are being studied as potential biomarkers for the early diagnosis of Parkinson’s disease and tracking the disease’s progression (Li and Le 2020). Parkin, VPS35, DJ1, PTEN-induced kinase 1, and leucine-rich repeat kinase 2 (LRRK2) are dangerous components that drive neuronal death in Parkinson’s disease (PD); these proteins help oxidative stress, inflammation, apoptosis, and dysregulated calcium homeostasis in neurons (Zimprich et al. 2004).
α-synuclein, a main bring on element for Parkinson’s disease, is coded by SNCA gene. Raised α-synuclein can cause excessive oxidative stress and distract calcium homeostasis, which can lead to dopaminergic neuron miscarriage in the brain of Parkinson’s disease patients (Lashuel et al. 2002). Pitx3 polymorphism is related with Parkinson’s disease (PD), and miR-133b acting a important role in Pitx3’s passive feedback control. Reduced expression of miR-133b letdowns the delicate equilibrium and eventually results in Parkinson’s disease. One of the degenerative alterations associated with Parkinson’s disease (PD) is oxidative stress, which is more sensitive to dopaminergic neurons when SNCA is highly expressed. Fibroblast growth factor 20 protein is levels is more when miR-433 expression is inhibited, which ultimately results in SNCA overexpression (Higgs and Lehman 2015). Alterations in the levels of miR-7 and miR-153 cause Parkinson’s disease (PD) and donate to the post-transcriptional mechanism of SNCA. AKT signaling pathway and phosphoinositide 3-kinase (P13K) be able to also cause overexpression of α-synuclein. Downregulate the P13K/AKT signaling pathway, stimulate miR-7 and miR-153 may perhaps be biomarkers related to the production of α-synuclein in Parkinson’s disease. Mutations in the LRRK2 gene can result in irregular and familial Parkinson’s disease (PD) disorders. LRRK2 is believed to be one of the most noteworthy proteins involved in the formation of dopaminergic neurons (Zimprich et al. 2004). Pointing the 3′-untranslated region (UTR) of LRRK2 mRNA, miR-205 and miR-599 can decrease LRRK2 levels and reduce MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-stimulate apoptosis in SH-SY5Y cells . In addition, through controlling oxidative stress and neuronal apoptosis in the cell, miR-34a, miR-153, and miR-626 are coupled to the different biological pathways in Parkinson’s disease. One of the important regulators of dopaminergic neuron homeostasis, the P13K/AKT, LRRK2/ERK1/2, and P13K/PTEN signaling pathways are disturbed with conditions like oxidative stress, neuronal death, and other pathophysiological mechanisms in Parkinson’s disease. Many miRNAs have been identified and optional to control neurodegeneration in Parkinson’s disease (PD), and these bioactive miRNAs could one day provide a stage for biological indicators and therapeutic targets(Li et al., 2023).