The long-standing focus of our research team has been on mechanisms of neurodegeneration and alpha-synuclein toxicity in Parkinson’s disease (PD). We have developed and characterized a variety of experimental models mimicking specific aspects of PD pathology and, for our work, we apply state-of-the-art histological and molecular biology techniques. Through these tools, we are investigating:

• the role of specific mechanisms, such as mitochondrial failure, protein degradation impairment, microglial activation and neuron-to-neuron protein transfer, in the pathogenesis of neurodegeneration and alpha-synuclein accumulation/aggregation in PD;
• how disease risk factors, such as aging, genetic variants and environmental exposures, can influence the onset and progression of PD pathology, and  
• the effectiveness of new therapeutic strategies (e.g., RNA silencing, immunotherapy and regenerative cell therapy) in preventing, slowing down or halting the pathological process underlying PD.

Although our research is mainly focused on PD, we are studying mechanisms and risk factors that are shared between PD and other neurodegenerative disorders. We believe that bridging different diseases will help us address key pathogenetic questions concerning, for example, mechanisms of selective neuronal vulnerability and conditions leading to clinical and pathological co-morbidity.