Our research activity is mainly focused on the general comprehension of the physiopathological mechanisms underlying neuroprotection or leading to neurodegeneration. We mostly use brain primary cultures and apply molecular biology and in vitro cellular approaches, including live cell imaging (calcium imaging and total internal reflection microscopy). We are interested in the way oxidative stress is generated and protection mechanisms are activated in both neurons and astrocytes. In light of the relevance of neuroinflammatory processes in neurodegeneration, interest is also directed to the molecular mechanisms involved in the process of glia activation and the influence the activated phenotype has on neuronal survival. At present, our research interests are mainly focused on two disease-oriented projects: I) Alzheimer's disease pathogenesis – Studies are in progress on: the regulation of BACE1/BACE2 expression; the implication of beta-secretase activity on amyloid-beta deposition; the cellular effects of the various amyloid-beta forms on different cell types from brain. II) Misregulation of intracellular iron homeostasis and hereditary neuroferritinopathy – We investigate the changes in cellular iron handling upon acute and chronic exposure to iron load and the ensuing production of Reactive Oxygen Species; a specific research line studies the effects of ferritin light chain mutations on cytosolic iron control.