I am currently a researcher within the Italian National Research Council (CNR), Neuroscience Institute, and I work at the Department of Biomedical Science at the University of Padua. I was previously affiliated with the CNR Institute of Biomedical Technologies (ITB) in Milan. The long-term interest of my work is mitochondrial pathophysiology, in particular the molecular characterization and functioning of the permeability transition pore (PTP), and, more recently, the role mitochondria play in neurodegenerative diseases such as Alzheimer's disease, concerning in particular Ca2+ dyshomeostasis, reactive oxidative species (ROS) production and metabolic imbalance I graduated from the University of Padua with a BSc Degree in Biology, and from the same University I earned a MSc. Degree in Biochemistry and Clinical Chemistry. I spent three years of postgraduate research in Molecular Biology at the Vollum Institute, the Oregon Health & Science University, Portland Oregon. From those years in the Pacific North West, together with a robust training in molecular biology, I gained also a love for outdoor sport activities, and in particular for biking.
From '87 to '91, I worked for my Ph.D. under the supervision of T. Pozzan. From '92 to '93, as an EMBO Fellow, I expanded my expertise in electrophysiology at the Max Plank Institut für Biophysikalische Chemie of Göttingen (Germany), under the supervision of R. Penner and M. Hoth. There, I participated in the characterization of the long sought after current responsible for capacitative Ca2+ entry (ICRAC), which they described in '92. In '96, I continued this research in the group directed by B. Nilius in Leuven (Belgium). In '98 I got a permanent position as Assistant Professor at the Dept of Biomedical Sciences (DBS), University of Padua. Here, I continued the characterization of ICRAC and Ca2+ stores in different model cells. In 2000, my interest turned to Ca2+ homeostasis in brain cells, under both physiological and pathological conditions. In recent years, I focused on mutant presenilins and their role in Ca2+ dysregulation and Alzheimer's disease.
I have mainly contributed to the study of the role played by the physical/functional connection between endoplasmic reticulum (ER) and mitochondria in the regulation of key intracellular processes, such as the modulation of cell death and cell bioenergetics. In particular, ER-mitochondria interplay has been investigated in the context of Familial Alzheimer’s disease. My research focused on the exploration of the molecular nature and of the relationship between proteins mediating ER-mitochondria tethering. I’m currently interested in the generation of novel tools to study organelles’ juxtaposition in living cells, as well as to investigate the mechanisms leading to the generation and deciphering of Ca2+ microdomains in localized subcellular compartments. In addition, by employing and creating specific genetically-encoded fluorescent probes, I’m investigating the dynamics (particularly within mitochondria) of different metabolites and signalling molecules (Ca2+, ATP, pyruvate, lactate, etc.), both in cell physiology and pathology. The final goal of my research activity is to understand whether alterations in these pathways are linked to the onset and progression of human pathologies, as well as to test their potential as possible therapeutic targets or as disease biomarkers.
I have a Ph.D. in Atomic and Molecular Photonics and a Master’s Degree in Biology (University of Florence). During my Ph.D., I focused on in vivo functional imaging in zebrafish larvae during visual stimulation with spectrally-distinct stimuli, investigating the processing of chromatic information in the whole larval brain and in the spinal cord. As a post-doc, I am currently involved in a project focused on the investigation of the role of mitochondrial Ca2+ dysregulation in mouse models of familial forms of Alzheimer’s diseases (FADs). I’m currently using two-photon calcium imaging of mouse brain slices, employing both wild-type and FAD-linked mutants at different stages of development, expressing the genetically-encoded Ca2+ indicators mt-GCaMP and jRGECO, for the concomitant measurement of [Ca2+] variation in mitochondria and cytosol.
Hi! I’m Paloma a post-doctoral researcher at Padova University. I studied Biology at Universidad Complutense de Madrid specializing in Neurobiology and Biomedical Sciences; afterwards I got a Master’s degree on Biomedical Sciences at the Universidad de Valladolid where my relationship with Ca2+ signaling research began studying Calcium dishomeostasis in aging and Alzheimer's disease in the Physiopathology of intracellular Calcium lab at the Institute of Biology and Molecular Genetics (IBGM). Then I got my PhD also at the University of Valladolid at the Aging and Calcium Signaling group (IBGM) where I investigated the possible use of Ca2+ signaling modulators as prolongevity drugs in the model organism Caenorhabditis elegans. During my PhD I also had the opportunity to do a three month visit to Dr. Malene Hansen's Lab at SBP, San Diego, CA, USA where I was able to increase my knowledge on autophagy in C. elegans. What to say about me... I´m from Spain, and I love live music, movies and traveling.
Over the last years, I have been involved in studying calcium (Ca2+) signaling in pathophysiology. My research focused on the development of new tools to explore the mitochondrial functionality, and in particular mitochondrial Ca2+ dynamics, in vivo. Therefore, I worked on the improvement of mitochondria-targeted Ca2+ probes and the creation of a new mitochondria-targeted Channelrhodopsin. These methodologies are instrumental for addressing with novel approaches the role of second messenger heterogeneity in different pathophysiological conditions not only in cell cultures, but also in tissue preparations (acute slices) and in vivo. Currently, I am interested in studying Familial Alzheimer's Disease (FAD), focusing on the imbalance of cellular Ca2+ homeostasis. Indeed, Alzheimer’s disease (AD) is the most frequent form of dementia, a small percentage of cases is inherited (FAD), due to dominant mutations in the genes encoding for Amyloid Precursor Protein (APP), Presenilin-1 (PS1) and Presenilin-2 (PS2). PS1 and PS2 are the catalytic core of the γ-secretase complex. Beside the current hypothesis about amyloid and tau hyperphosphorylated, cellular Ca2+ alterations have been reported to contribute to the AD pathogenesis, however this topic is still debated in the scientific community. The final goal is the employment of these newly created tools to perform in vivo Ca2+ measurements in different tissues and subcellular compartments in animal models of AD.
Diana Pendin is a Researcher at the Neuroscience Institute of the National Research Council since 2018. Her research aims to untangle the molecular basis of the pathogenesis of the neurodegenerative disease Hereditary Spastic Paraplegia (HSP), using Drosophila melanogaster as an animal model. Since the very beginning of her career, she has been particularly interested in understanding how ER morphology alterations affect cellular, and more specifically neuronal, function. Recently, she explored the role of Ca2+ homeostasis dysregulation in the development of HSP by employing Ca2+ imaging techniques. She also contributed in developing novel tools to study in vivo Ca2+ dynamics, including viral vectors and transgenic animals (mice and Drosophila) expressing FRET-based Ca2+ probes.
I graduated in Biological Sciences in 1988, with full marks, at the University of Padua, Italy. In 1993, at the University of Bologna, Italy, I obtained my Ph.D. in Experimental Pathology, working in the laboratories of Prof. Francesco Di Virgilio and Prof. Giovanni Salviati. Afterwards, thanks to the support of EMBO (short-term fellowship) and Telethon, I was a post-doc at the Weizmann Institute of Science, Rehovot, Israel, in the laboratory of Prof. David Yaffe, working on a new product of the dystrophin gene, the Dp71 protein. Returning to Padua, I joined the lab of Prof. Tullio Pozzan at the University’s Institute of Pathology, working first as a research assistant and later as an academic researcher. In 2012, I was a visiting scientist for two months at the Institute of Neuroscience, University of Oregon, USA, in the laboratory of Dr. Philip Washbourne. In 2014, I was appointed Associate Professor of General Pathology, School of Medicine, University of Padua. In my free time, I enjoy staying with my family, walking or skiing in the Dolomites, and swimming with a master team in my city.
Post-doc researcher at the Neuroscience Institute of CNR. I have a master’s degree in Pharmaceutical Biotechnology and a PhD in Biomedical Sciences. I focused my PhD work on studying how structural changes of the Endoplasmic Reticulum (ER), caused by a Hereditary Spastic Paraplegia (HSP)-linked mutant form of spastin, affects calcium homeostasis in Drosophila melanogaster. As a Post-doc, beside further exploring how other HSP-inducing mutations affect the structure and function of ER, I am currently involved in the development and characterization of organelle-targeted calcium probes.