Neuroprotective potential of Epigenetic modulators, its regulation and therapeutic approaches for the management of Parkinson's disease.

The progressive degeneration of dopaminergic neurons in the substantia nigra region of the brain leads to a deficiency of dopamine and, ultimately, the onset of Parkinson's disease (PD). Since there is currently no cure for PD, patients all around the world are dealing with symptomatic management. PD progression is influenced by multiple elements, such as environmental, biological, chemical, genetic, and epigenetic factors. Epigenetics is gaining increased attention due to its role in controlling the expression of genes that contribute to PD. Recent advancements in our understanding of the brain network and its related conditions have shown that alterations in gene expression may occur independently of genetic abnormalities. Therefore, a thorough investigation has been carried out to explore the significance of epigenetics in all degenerative disorders. Epigenetic modifications are essential for regulating cellular homeostasis. Therefore, a deeper understanding of these modifications might provide valuable insights into many diseases and potentially serve as targets for therapeutic interventions. This review article focuses on diverse epigenetic alterations linked to the progression of PD. These abnormalities are supported by numerous research on the control of gene expression and encompass all the epigenetic processes. The beginning of PD is intricately associated with aberrant DNA methylation mechanisms. DNA methyltransferases are the enzymes that create and preserve various DNA methylation patterns. Integrating epigenetic data with existing clinical methods for diagnosing PD may aid in discovering potential curative medicines and novel drug development approaches. This article solely addresses the importance of epigenetic modulators in PD, primarily the mechanisms of DNMTs, their roles in the development of PD, and their therapeutic approaches; it bypasses other PD therapies.