Genetic and Epigenetic Collaboration in Parkinson’s disease

Parkinson's disease (PD) is a common neurodegenerative syndrome that progreses with age and presents in many forms. Some efforts to understand PD development include regulation of epigenetic mechanisms, which usually include minor molecular modifications of DNA and histones which are essential to regulate genetic activity. We have highlighted the problems associated with the development of genetic and epigenetic processes and reviewed several studies. None of these led to stronger conclusions about the autonomous roles of epigenetic pathways. Data from the current standpoint suggests that SNCA, one of the hallmark genes implicated in PD, is more prevalent than pathways that directly require DNA methylation, as a consequence of complicated DNA hydroxymethylation, global hyperacetylation, and histone deacetylase (HDAC). Without current epigenetic clinical goals to delay PD progression, we hypothesize how PD neurons, with the potential therapeutic objectives, can affect local and global epigenetics via inflammation, oxidative stress, autophagy and DNA repair mechanisms.