Education and Training
1994         Degree in Physics, University of Genova, Italy
1995-1997    Graduate Fellow, Dept. of Biological Chemistry, University of Padova, Italy
1997-2000     Ph.D. in Biochemistry and Biophysics, University of Padova, Italy
2000-2002    Post-doc Fellow, Dept. of Neuroscience, Istituto di Ricerche Farmacologiche “M. Negri”, Milano, Italy

Academic Position
2002-present    Research Associate, Dept. of Biomedical Science, University of Padova

My early scientific activity was carried out in the laboratory of Dr. Franco Conti at the Institute of Cybernetics and Biophysics (CNR) in Genova, and was addressed to the electrophysiological characterization of mammalian CNS ion channels. Starting from 1995, when I joined the group of Dr. Catia Sorgato at the Dept. of Biological Chemistry, University of Padova, I was involved in the study of mitochondrial ion channels. As a PhD student, my major scientific interest moved to the physiopathology of the prion protein (PrP). In particular, I studied the cellular metabolism of some mutant forms of PrP associated to human prion diseases. From 2000 to 2002 I held a post-doctoral position in the laboratory of Dr. Gianluigi Forloni at the Research Institute Mario Negri (Milano, Italy). During this period, I was mainly interested in the molecular mechanisms of Parkinson’s disease, and I took part to other research projects on the molecular and cellular basis of different neurodegenerative disorders. Starting from December 2002, I hold a position as Research Associate at University of Padova. In recent years, I was involved in different research projects on PrP and prions. These included the study of soil contamination by prions, which resulted in the development of a method to detect directly prions in soil samples, and the investigation of the physiologic role of PrP, which has also been pursued by means of ex-vivo and in-vivo muscle paradigms and the analysis of local Ca2+ movements in primary neurons. More recently, my scientific interest moved to the pathogenic mechanisms of amyotrophic lateral sclerosis, with particular emphasis to the involvement of Ca2+ de-regulation and ER and mitochondrial dysfunctions in the disease onset.

At present, my major research interest deals with the possibility that local perturbations of Ca2+ homeostasis, and related ER and mitochondrial dysfunctions, play an early role in ALS pathogenesis. This is mainly studied in primary cell cultures of motor neurons and astrocytes from the spinal cord of transgenic mice.
WHAT IS ALS? Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective death of motor neurons (MNs) in the motor cortex, brainstem and spinal cord. In most cases ALS occurs sporadically, but 10% of the cases show a familial history and about 20% of these familial forms are caused by a mutation in the superoxide dismutase-1 (SOD1) gene.
RESEARCH OUTLINE. Following novel observations that mutant SOD1 alters signaling pathways and Ca2+ fluxes in MNs, we aim at verifying if perturbed Ca2+ homeostasis in the endoplasmic reticulum (ER) is prodromal to ER stress, which is regarded as central to ALS pathogenesis. We will also consider the possibility that altered ER Ca2+ homeostasis affects mitochondrial Ca2+ fluxes, amplifying in this way deadly signals to MNs. These goals are pursued by analyzing local Ca2+ fluxes with Ca2+-sensitive probes genetically targeted to specific cell domains of primary MNs expressing the human ALS-related SOD1G93A mutant, or the wild-type (WT) counterpart. Studies include a stringent focus on store-operated Ca2+ entry that links ER Ca2+ levels to the control of neuronal overall Ca2+ handling and excitability. A consistent part of the project also aims at understanding if SOD1G93A astrocytes have deranged local Ca2+ movements, and if this contributes to MN disease.
MAIN METHODOLOGIES. The main cell model systems consists of primary cultures of MNs and astrocytes from transgenic mice, and the immortalized MN cell line NSC-34, expressing human SOD1WT or SOD1G93A. The analysis of local Ca2+ movements exploits Ca2+ probes (aequorins and/or cameleons), genetically targeting different cell compartments (cytoplasm, cytosolic sub-plasma membrane domains, ER lumen and mitochondrial matrix), and expressed through plasmidic or lentiviral vectors also containing MN- or astrocyte-specific promoters. In parallel to Ca2+ measurements, several other functional parameters of the ER and mitochondria are analysed by means of different techniques

AriSLA (Agenzia di Ricerca sulla Sclerosi Laterale Amiotrofica): LoCaLS – “Local perturbations of Ca2+ homeostasis as possible early mechanisms of fALS pathogenesis” (€ 59997; end: March 2015)