• Parkinson's disease
• mitochondrial dysfunction

The main focus of the project is the characterization of mitochondrial dysfunction in neural cell models of Parkinson’s disease (PD).
The first purpose is to investigate how Rotenone and H2O2 reproduce a PD-related cell damage. Using viability assays, MTT and Neutral Red, is then observed how these substances modulate the cells death.
Secondary how mitochondrial impairment influences mitochondrial associated proteins, DJ-1 and Nrf2, linked to the pathophysiology of PD. Loss of DJ-1 is recruited by mitochondria under conditions of oxidative stress and can influence the translocation of Nrf2 to the nucleus to activate the antioxidant response element. Defects in DJ-1 have been identified in some familial forms of Parkinson’s disease and impairment of the antioxidant response are strongly linked to idiopathic cases. The effect of specific PD-related neurotoxins mitochondrial associated proteins has also been studied using methods such as tissue culture, SDS-PAGE gel electrophoresis and Western blotting.
At last the project is extended to investigate the molecular events that occur during mitochondrial dysfunction and whether this phenomenon can be modulated to maintain neuronal cell survival. In particular has been analysed how the growth factors produced by Glioma cells culture modules the neuronal viability, in normal grow conditions as in neurotoxic conditions. The role that these factors may play in maintaining glial cell function is also of interest since these cells provide significant support to the dopaminergic neurones that are targeted in Parkinson’s disease.