PRIN 2022 MEANT - Energy Metabolism: a new target for Neuroprotective Strategies in Parkinson's Disease

It is increasingly known that dysregulation of neuronal mitochondrial energy metabolism is implicated in neurodegeneration and the pathogenesis of Parkinson’s disease (PD). Oxidative damage to mitochondrial proteins and organelles can compromise neuronal energy balance and ATP production, resulting in cellular apoptosis. Indeed, some studies demonstrate that dopaminergic (DA) neurons in the substantia nigra (SN) are characterized by high energy demands, making them extremely vulnerable to neurodegeneration. This can trigger damage to mitochondrial energy metabolism in tissues and systems with high energy demands, resulting in a neuroinflammatory process that represents the critical point in disease progression.

This project aims to investigate energy metabolism dysfunction in the pathophysiology of Parkinson’s disease and define a promising intervention (drugs and new alternative compounds based on fermented vegetables and cereals) that, by rescuing the initial pathological processes, can slow or prevent neuroinflammation and/or neurodegeneration.