Curriculum in PDF: English CV

My laboratory is interested in studying the molecular mechanisms underlying the early events of neurodegeneration associated with Parkinson’s disease. We are particularly focused on the pathophysiology of the kinase LRRK2, whose mutations represent the single most common cause of familial Parkinson’s disease, on glucocerebrosidase (GBA), a lysosomal enzyme that mutated represents the most important risk factor for Parkinson's disease, and on SPG11, a lysosomal protein mutated in a familial form of Hereditary Spastic Paraplegia with parkinsonism. We combine cellular and animal models to investigate the signaling pathways and the pathological consequences of gene mutations on neuronal and glial cells homeostasis.

1. Role of the Parkinson’s disease kinase LRRK2 in shaping neurites and synapses 2. Neuronal signalling associated with the kinase PAK6 3. Role of 14-3-3 proteins in the neuronal regulation of TFEB, the master coordinator of autophagy and lysosome biogenesis 4. Role of SPG11, a protein mutated in Hereditary Spastic Paraplegia, in the autophagy-lysosomal pathway 5. Regulation of GBA activity, subcellular localization and lysosomal function by LRRK2