Fig.1: ER-mitochondria contacts in Control and Familial Alzheimer’s disease (FAD) fibroblasts carrying the N141I mutation in PS2.

1988: graduated with full marks in Biological Sciences at the University of Padua, Italy.

1989-1993: Ph.D. in "Experimental Pathology", at the Institute of General Pathology, University of Padua, Italy.

1993-2001: research associate at the Department of Biomedical Sciences, University of Padua, Italy

2001-2014: Assistant Professor, General Pathology, School of Medicine, University of Padua, at the Department of Biomedical Sciences, Italy

January 2014: National Academic Qualification as Associate and Full Professor of General Pathology

October 2014: Associate Professor, General Pathology, School of Medicine, University of Padua, at the Department of Biomedical Sciences, Italy

International Experience:

1992-1993: Visiting scientist at the Weizmann Institute of Science, Rehovot, Israel, in the laboratory of Prof. David Yaffe.

2012 July-August: Visiting scientist at the Institute of Neuroscience, University of Oregon, USA, in the laboratory of Dr. Philip Washbourne.

2013 July-August: Visiting scientist at the McKusick-Nathans, Institute of Genetic Medicine, Johns Hopkins University Baltimore, USA, in the laboratory of Prof. Steven Leach.


1992: EMBO short term fellowship recipient at the Weizmann Institute of Science, Rehovot, Israel.

1993: Telethon fellowship recipient for the study of neuromuscular diseases, at the Weizmann Institute of Science, Rehovot, Israel, in the laboratory of Prof. David Yaffe.

The main scientific interest of Dr. Pizzo regards the mechanisms of Ca2+ homeostasis in mammalian cells and the role of Ca2+ as second messenger in cellular physiopathology.

In the last 10 years she has started a project on Ca2+ dysregulation in Familial Alzheimer’s disease (FAD). In particular, using different disease cell models, it has been defined how FAD-linked mutated forms of presenilin 2 (PS2) alter cellular Ca2+ handling, reducing the intracellular Ca2+ store content but increasing the mitochondrial Ca2+ uptake. Her research pointed out that PS2, indeed, is able to modulate the tethering between mitochondria and the endoplasmic reticulum (ER), the major intracellular Ca2+ store, with its FAD mutants increasing it and thus favouring mitochondria Ca2+ uptake upon ER Ca2+ release. Her studies are now aimed to understand whether and how this new PS2 function might be involved in the pathogenesis of the disease altering, for instance, mitochondria physiology.

Dr. Pizzo collaborates with Dr. Pozzan on research projects dealing with Ca2+ handling by different intracellular organelles, using a new family of probes, genetically encoded, based on FRET (Fluorescence Resonance Energy Transfer), and with several other groups to study the role of Ca2+ in diverse physio-pathological processes. She has published more than 70 papers in international journals.

  1. Zampese E., Fasolato C., Kipanyula M.J., Bortolozzi M., Pozzan T. and Pizzo P. (2011). “Presenilin 2 modulates ER-mitochondria interactions and Ca2+ cross-talk”. Proc Natl Acad Sci U S A., 108: 2777-82.
  2. Giacomello M., Drago I., Bortolozzi M., Scorzeto M., Gianelle A., Pizzo P. and Pozzan T. (2010). “Ca2+ hot spots on the mitochondrial surface are generated by Ca2+ mobilization from stores, but not activation of store operated Ca2+ channels”. Molecular Cell, 38:280-90.
  3. Brunello L., Zampese E., Florean C., Pozzan T., Pizzo P.* and Fasolato C. (*corresponding author) (2009). “Presenilin-2 dampens intracellular Ca2+ stores by increasing Ca2+ leakage and reducing Ca2+ uptake”. J Cell Mol Med., 13:3358-69.
  4. Florean C., Zampese E., Zanese M., Brunello L., Ichas F., De Giorgi F. and Pizzo P. (2008). “High content analysis of g-secretase activity reveals variable dominance of presenilin mutations linked to familial Alzheimer's disease”. BBA - Molecular Cell Research, 1783:1551-60.
  5. Giacomello M., Barbiero L., Zatti G., Squitti R., Binetti G., Pozzan T., Fasolato C., Ghidoni R. and Pizzo P. (2005). “Reduction of Ca2+ stores and Capacitative Ca2+ Entry is associated with the Familial Alzheimer’s Disease presenilin-2 T122R mutation and anticipates the onset of dementia”. Neurobiology of Disease, 18, 638-648.

Link to complete list of publications (PDF).

Grant CARIPARO “Excellent Project” 2011-2012, “The endoplasmic reticulum-mitochondria connection: role in cell physiology and pathology”.

2-year post-doct fellowship, University of Padua, “Role of Presenilin 2 in the endoplasmic reticulum-mitochondria tethering”.

GRANT Europeo Joint Program in Neurodegenerative Disease 2015-2018, "Cellular Bioenergetics in Neurodegenerative Diseases: A system-based pathway and target analysis "