Historically, our lab has been interested in calcium (Ca2+) homeostasis and its role in cell signalling, in both health and disease. In the last years, different projects centred on cellular Ca2+ handling in Alzheimer’s Disease (AD) were started. By analysing different familial AD cell and mouse models, expressing presenilin 2 (PS2) mutants, we have characterized alterations in intracellular Ca2+ handling, mitochondria function and brain network excitability, all features potentially linked to disease pathogenesis.
Another major topic of the lab over the last years has been the development and use of organelle targeted GFP-based fluorescent indicators for monitoring Ca2+ dynamics in living cells. These new tools, targeted to different organelles, such as Endoplasmic Reticulum (ER), Golgi apparatus, mitochondria, peroxisomes, have allowed, for the first time, to address the study of Ca2+ homeostasis in subcellular compartments for which only indirect information was available.
In addition to Ca2+, the interest of our group is also concentrated on cAMP signalling. In this context, novel tools − again targeted to subcellular regions (plasma membrane, mitochondria, nucleus) − have been generated and characterized and several signalling pathways linked to this second messenger have been detailed.
All these methodologies are used to address with novel approaches the role of second messenger heterogeneity in different physio-pathological conditions (e.g., the control of cardiac cell excitability or the pathogenesis of AD) not only in cell lines or primary cell cultures, but also in tissue preparations (acute slices) and in vivo.
