1983, graduated with full marks in Biological Sciences at the University of Padua, Italy

1984-86, research associate at the Institute of Biological Chemistry, University of Padua, Prof. L. Galzigna.

1987-91, PhD in "Molecular and Cellular Biology and Pathology" of the University of Padua, Mentor T. Pozzan.

1994-95 research associate at the Dept Biomedical Sciences (DBS), University of Padua, Italy.

1998-present assistant professor in Physiology, School of Pharmacy, DSB, University of Padua, Italy.

International Experience:

1992-93 EMBO Fellowship recipient at the MPI für Biophysikalische Chemie, Göttingen, Germany,

Mentor R. Penner.

1996-97 Fellowship recipient at the Dept Molecular and Cellular Biology, Catholic University of Leuven,

Belgium, Mentor B. Nilius.

From ’87 to ’91, I worked for my PhD under the supervision of Tullio Pozzan, a world experts in Ca2+ imaging and cAMP signal transduction, using both classical and genetically encoded probes. From ’92 to ’93, as an EMBO Fellow, I expanded my expertise in electrophysiology at the Max Plank Institut für Biophysikalische Chemie, Göttingen, Germany, directed by Nobel Laureate Erwin Neher. There, I participated in the characterization of the calcium‑release‑activated Ca2+ current (ICRAC), the long‑sought‑after current responsible for capacitative calcium entry, described in ’92 by Reinhold Penner and Markus Hoth. In ’96 I went to Leuven, Belgium, working in the group directed by Bernd Nilius, an internationally recognized expert in electrophysiology and molecular biology.

In ’98 I got a permanent position as assistant professor in Physiology at DBS in Padua. Here, based on the accumulated experience in electrophysiological recordings coupled to Ca2+ imaging, I continued the characterization of ICRAC and Ca2+ stores in different model cells, in collaboration with Tullio Pozzan. In 2000, my interest turned to Ca2+ homeostasis in brain cells, under physiological as well as pathological conditions. During the last decade, Paola Pizzo and I started a project on Ca2+ dysregulation in Familial Alzheimer’s disease (AD). We discovered that presenilin-2, which is mutated in familial AD, alters cellular Ca2+ handling, by reducing the Ca2+ content of intracellular stores and increasing the mitochondrial Ca2+ uptake, an effect independent of oligomeric amyloid-beta species. In collaboration with Stefano Vassanelli at DBS, we recently identified altered slow oscillations as an early marker of cortico-hippocampal dysfunctions in pre-deposition AD mice carrying mutant PS2 and low/high power imbalance in plaque-seeding AD mice.

2012: associate professor habilitation, 05/D1 Physiology, MIUR, Italy.
1998-present: assistant professor of Physiology, University of Padua, Faculty of Pharmacy.
1998: editor, with R. Rizzuto, of the book "Imaging living cells", published by Springer-Verlag, Heidelberg.
2003-present: member of the School of Doctorate in Biosciences, University of Padua

Referee for international scientific journals:
J. Cell Biol., Eur. J. Neurosci., Cell Calcium, Eur. J. Pharmacol., Eur. J. Biochem., J. Physiol. London,
J. Neurochem., J. Biol. Chem., Molecular Neurodegeneration, Cells, IJMS, Scientific Report, Aging Cell.

Scientific Society Membership:
Italian Society of Neurosciences (SINS); Italian Association of Cellular Biology and Differentiation (ABCD)
Trisomy 21 Research Society (T21RS).

A. Leparulo, M. Mahmud , E. Scremin, T. Pozzan, S. Vassanelli S, C. FasolatoDampened Slow Oscillation Connectivity Anticipates Amyloid Deposition in the PS2APP Mouse Model of Alzheimer's Disease.” Cells 2020, 9(1) pii: E54. doi: 10.3390/cells9010054 (2020) 9(1), 54.

R. Fontana, M. Agostini, E. Murana, M. Mahmud, E. Scremin, M. Rubega, G. Sparacino, S. Vassanelli and C. Fasolato (2017) “Early hippocampal hyper-excitability in PS2APP mice: role of mutant PS2 and APP” Neurobiology of Aging 50, 64-76.

M. Agostini and C. Fasolato (2016) “When, where and how? Focus on neuronal calcium dysfunctions in Alzheimer's Disease” Cell Calcium Nov;60(5):289-298. doi:10.1016/j.ceca.2016.06.008. Review.

C. Lazzari, M.J. Kipanyula, M. Agostini, T. Pozzan and C. Fasolato (2015) Aβ42 oligomers selectively disrupt neuronal calcium release. Neurobiology of Aging 36, 877-885

M.J. Kipanyula, L. Contreras, E. Zampese, C. Lazzari, A.K.C. Wong, P. Pizzo, C. Fasolato (corresponding author) and T. Pozzan (2012) Ca2+ dysregulation in neurons from transgenic mice expressing mutant presenilin 2. Aging Cell 11, 885–893 ISSN: 1474-9718, doi: 10.1111/j.1474-9726.2012.00858.x.

PRIN-20175C22WM “Early dysfunctions of intercellular signalling in brain disorders" to T. Pozzan, Collaborator

UniPD Fellowship grant BIRD171870/17 PI

CARIPARO Foundation. Excellence project 2017 (2018/113) to T. Pozzan, Collaborator

PRIN-2015W2N883 PRIN - Bando 2015 - "Astrocytes in brain pathophysiology: focus on calcium signalling” to T Pozzan, Collaborator

Atheneum Research Project CPDA157003/15 “Astrocyte calcium imbalance and hippocampal network activity in Alzheimer’s disease mouse models based on mutant presenilin 2” PI

CNR Ageing Project 2012-16 “Studies of molecular mechanisms of neurodegeneration” to T. Pozzan Collaborator

Altered brain oscillatory activity in the double transgenic (2TG) PS2APP mouse model of Alzheimer’s disease.

Amyloidosis and gliosis in a sagittal section of 6-month-old PS2APP mice. At the hippocampal (CA1) and cortical levels, plaques, stained by anti-amyloid-β antibody (red) are surrounded by activated astrocytes, stained by GFAP antibody (green) and nuclei stained by NucRed (blue), scale bar = 0.3 mm. B,C. With respect to wild-type (WT), 2TG mice show power imbalance between Low and High frequency oscillations, measured by recording Local Field Potential with a multisite linear probe (Leparulo et al. 2020).