InflammaPark PROJECT

FRRB Project 1750818 - Decoding the molecular basis of the interplay between neuroinflammation and neurodegeneration in Parkinson’s disease

PROJECT SUMMARY

Parkinson's disease (PD) affects approximately 0.3% of the Italian population, a percentage that rises to 1% for individuals over 50 years old. Currently available treatments are purely symptomatic and have no impact on the progression of the disease. This, combined with the progressive aging of the population, leads to an increase in healthcare expenses. Taking prompt action on the possible causes of the disease represents a promising strategy as it allows for the cessation or slowing down of the processes that lead to irreversible neuronal death. In the early stages of PD, there is a strong inflammatory component in the brain, which appears to play a crucial role in the development of the condition. This inflammation, through mechanisms involving the immune system, seems to contribute to the creation of a toxic local environment for neurons, increasing their vulnerability. The aim of this study is to understand the mechanisms involved in inflammation-mediated toxicity, with the goal of developing therapies to resolve or attenuate the processes that lead to PD development. The results obtained so far clearly indicate that the immune system actively participates in the neurodegenerative process of PD, giving rise to chronic inflammatory processes that contribute to the death of dopaminergic neurons. These findings suggest that an approach aimed at reducing or blocking neuroinflammation could be highly beneficial in slowing down the progression of the disease. To this end, this project has identified an anti-inflammatory molecule known as interleukin-10, which has been shown to modulate the immune response in inflamed tissue and thereby reduce neuronal degeneration. The results obtained thus far provide a solid foundation for the development of targeted therapies that could bring significant benefits to the management of PD.