Marco Mainardi

Marco Mainardi is an Associate Professor of Physiology at University of Padua.

 

His training in biological research started with a master’s degree in molecular biology at University of Pisa (2006), where he also received an Honors degree in Biology after completing the graduate course at Scuola Normale Superiore. Then, he received his PhD Neuroscience, still from Scuola Normale Superiore (2010), after working under the supervision of prof.s Lamberto Maffei, Matteo Caleo, and Tommaso Pizzorusso on the effect of environmental stimuli on synaptic plasticity, using in vivo electrophysiology, imaging, and biochemistry. He then continued to explore these topics with a postdoc at the Neuroscience Institute of the National Research Council. In 2014, he moved to the Physiology Institute of Catholic University in Rome with an assistant professor position. While getting proficient in patch-clamp electrophysiology and coimmunoprecipitation techniques, he contributed to elucidate the effect of metabolic stressors, such as a hyperlipidic diet, in curbing synaptic plasticity. In 2017, Marco moved back to Scuola Normale Superiore, where he became assistant professor in Antonino Cattaneo’s lab, where he was introduced to the design and validation of genetically encoded tools for synapse labeling and analysis, which he used to create maps of in vivo synaptic plasticity in the hippocampus, as well as to analyze the variations in the molecular composition of synapses in response to learning. In 2019, Marco obtained his first independent position as a researcher of the Neuroscience Institute of the National Research Council, where he was promoted senior investigator before moving to University of Padua in 2023.

 

Marco’s current research interests are focused on understanding how synapses are affected by physiological variations in sensory inputs as well as by pathological states, including Alzheimer’s disease and neuroinflammation. To answer his scientific questions, he employs a combination of genetically encoded reporters and probes, behavioral testing, electrophysiology, imaging, and biochemistry in preclinical models. His research is supported by grants from the Ministry of University and Research, as well as from private charities, such as AirAlzh (Italian Association for Research on Alzheimer’s).

 

Marco’s ultimate goal as a researcher is to make contributions which can be truly useful to ameliorating the condition of diseased people, by exploiting basic research to indicate new potential targets for the therapy of neurodevelopmental and neurodegenerative diseases.

 

Scopus link: https://www.scopus.com/authid/detail.uri?authorId=26424686300
Google Scholar link: https://scholar.google.it/citations?user=hkEBXloAAAAJ&hl=it

Tito Calì

Tito Calì is Full Professor at the Department of Biomedical Sciences, University of Padova.

 

2017: Assistant Professor, (RTDB) Department of Biomedical Sciences, University of Padova.

2015-2016: Assistant Professor, (RTDA) Department of Biomedical Sciences, University of Padova.

2013-2015: Senior Research Associate, University of Padova.

2009-2013: Junior Research Associate, University of Padova.

2008: PhD Degree “in signi cum laude”, Biochemistry/Molecular Biology, Theodor Kocher institute, University of Bern (CH) and Institute for Research in Biomedicine (IRB), Bellinzona (CH).

2005: Doctor in Biological Sciences 110/110 “Cum Laude”, Biochemistry/Molecular Biology, University of L’Aquila and Centre d’Immunologie Marseille Luminy (CIML).

 

Selected Publications

Calì T, et al. The ataxia related G1107D mutation of the plasma membrane Ca2+ ATPase isoform 3 affects its interplay with calmodulin and the autoinhibition process. BBA. 2017

Calì T, et al. A new split-GFP-based probe reveals DJ-1 translocation into the mitochondrial matrix to sustain ATP synthesis upon nutrient deprivation. HMG. 2015.

Calì T, et al. A Novel Mutation in Isoform 3 of the Plasma Membrane Ca2+ Pump Impairs Cellular Ca2+ Homeostasis in a Patient with Cerebellar Ataxia and Laminin Subunit 1? Mutations. JBC 2015.

Calì T, et al. Enhanced parkin levels favor ER-mitochondria crosstalk and guarantee Ca2+ transfer to sustain cell bioenergetics. BBA. 2013

Calì T, et al. ?-Synuclein controls mitochondrial calcium homeostasis by enhancing endoplasmic reticulum-mitochondria interactions. JBC. 2012

Zanni G, Calì T, et al. Mutation of plasma membrane Ca2+ ATPase isoform 3 in a family with X-linked congenital cerebellar ataxia impairs Ca2+ homeostasis. PNAS. 2012

Micaela Zonta

Micaela Zonta is Research Technologist at the Neuroscience Institute of the National Research Council in Padova.

 

She obtained her degree in Biology at the University of Padova and her PhD under the supervision of the CNR neuroscientist Giorgio Carmignoto, investigating how calcium signal in astrocytes regulates gliotransmitter release and functional hyperemia.

 

Her research group at the CNR Neuroscience Institute in Padua investigates the role of astrocytes in Alzheimer’s Disease mouse models and in the modulation of dopaminergic circuits.

 

Research interests
Our research interests focus on the characterization of Ca2+ signals in astrocytes from different brain circuits and in different brain pathological states. To pursue our aims, we combine 2 photon imaging, electrophysiological techniques and immunohistochemistry.

 

Our recent results reveal the contribution of astrocytes to synaptic modulation in the dopaminergic circuits of Ventral Tegmental Area, and the effects of early astrocyte Ca2+ dysregulation on somatosensory synaptic plasticity in a mouse model of Alzheimer’s disease (B6.152H).

 

We are actually studying Ca2+ signals in hippocampal astrocytes from α7 nicotinic acetylcholine receptor knockout mice, characterized by an age-dependent Alzheimer’s disease-like phenotype, and in parallel we are deepening Ca2+ signal characterization in astrocytes from the Ventral Tegmental Area.

 

In a recently funded Telethon project, we are exploring cerebrovascular function in the B6.152H Alzheimer’s mouse model, to disclose possible links existing between the impairment observed in astrocyte Ca2+ signal and the different aspects of vascular dysfunction commonly reported in Alzheimer’s disease.

 

ORCID: https://orcid.org/0000-0002-9982-6405

Morten Gram Pedersen

Morten Gram Pedersen is Associate Professor in Bioengineering at the Department of Information Engineering, University of Padova.

 

He leads the unit for Modeling of Cell Biology. He holds a PhD in Mathematical Biology from the Technical University of Denmark, and has obtained independent funding for several postdoc positions, including a EU Marie Curie Intra-European Fellowships with Lund University Diabetes Centre, Malmö, Sweden.

 

He is the author of more than 50 papers on peer-reviewed journals (or which 8 as single author, 17 as first author; 30 as corresponding author). Besides collaborations with researchers from several departments of the University of Padova (Depts. Biomedical Sciences, Physics, Medicine, Mathematics), among others, he collaborates with experimental and theoretical researchers at Oxford University, UK; Uppsala University, Sweden; University of Exeter, UK; National Institutes of Health, MD, USA; Florida State University, FL, USA.

 

His main interests are mathematical modeling and theoretical analysis of:

  • local, intracellular calcium dynamics
  • local control of calcium-dependent potassium channels
  • protein and calcium dynamics evoking exocytosis of secretory vesicles
  • electrical activity in neuro-endocrine cells
  • clusters of electrically coupled cells