Education: 2006 Doctor of Philosophy in Neuroscience, Faculty of Medicine and Biological Sciences, Leicester University (UK), (Supervisor: Professor Pierluigi Nicotera). 2001 Laurea degree in Biological Sciences, University of Padova (Italy). Final score: 110/110 Research and Professional Experience: 2014-present Assistant Professor, Department of Biology, University of Padova, Italy 2012-2014 Boursieres d’Excellence, Marie Curie Action Fellow. Faculté de médecine de Genève, University of Geneva, Switzerland 2011-2012 Boursieres d’Excellence, EMBO long term Fellow. Faculté de médecine de Genève, University of Geneva, Switzerland 2007-2011 Post Doctoral scientist. Medical Research Council (MRC), Centre for developmental and biomedical genetics. UK, Sheffield. (Neuroscience, Prof. A. Whitworth). 2006-2007 Post Doctoral scientist. Medical Research Council (MRC), Toxicology Unit. UK, Leicester. (Neuroscience, Prof. P. Nicotera). 2001-2006 PhD Student. Medical Research Council (MRC), Toxicology Unit. UK, Leicester. (Neuroscience, Prof. P. Nicotera). 2000-2001 Internship Student. Department of Histology Microbiology and Medical Biotechnologies. University of Padua, Italy (Development, Prof. S. Piccolo). Awarded Fellowships: Feb 2012-2014 Marie Curie Action Feb 2011-Feb 2012 EMBO Long Term Sept 2006-Sept2007 MRC Special Award for outstanding contribution to the work of the MRC Toxicology Unit over the year 2006. Research Support: 2015-2016 Michael J Fox Foundation, RRIA (Co-PI; 125,000 $) 2014-2015 Michael J Fox Foundation, RRIA (PI; 75,000 $) 2014-2017 “Brain Gain” grant, Italian Ministry of Health (PI; 232,000 €) 2014-2017 “Ricerca Finalizzata” grant, Italian Ministry of Health (PI; 342,088 €) 2015-2017 Marie Curie- Padova University co- funded program (PISCOPIA program), which was granted to Dr Joy Chakraborty, former post doc in Ziviani lab (Supervisor; 73,218€) 2015-2017 Grant to cover a 2-years Junior postdoctoral fellowship, University of Padova (40,000€). 2015-2016 Ricerca Scientifica fondi quota EX 60% Anno 2015 (PI, 3291€). Anno 2016 (PI, 4569€) 2013-2014 Parkinson Schweiz grant for the promotion of scientific Parkinson’s Research (PI; 25,000 CHF) Graduate Students and researcher supervision: 2015-Present Dr Sophia Von Stockum, Post Doctoral scientist, Dr Joy Chakraborty, Marie Curie-University of Padova co- funded (Piscopia program) Post Doctoral Fellow, Dr Olivier Ek, Junior Post doctoral Fellow, 2015-Present Miss Elena Marchesan, internship student, Department of Biology, University of Padova, Italy. Review Editor: Frontiers in Cellular Neuroscience, Biology Direct Regular Reviewer activity: Cell Death and Differentiation Cell Death and Disease Physiological Genomics The Journal of Neuroscience Grant reviewing activity 2016 Ad hoc peer review, Michael J. Fox foundation 2016 Ad hoc peer review, Parkinson’s UK

Curriculum in PDF: English CV

Dr Elena Ziviani has a broad background in Neuroscience, with specific training and expertise in molecular biology, in vitro primary neuron culture and in vivo experimentation, both in mice and in Drosophila Melanogaster fruit fly. Dr Ziviani accomplished her PhD in Neuroscience at the MRC toxicology Unit in Leicester, UK, under the supervision of Professor P. Nicotera where Elena investigated the effect of nicotine in primary neurons on neuroprotection and synaptic plasticity. In November 2007, Dr Ziviani joined Dr. Alex Whitworth’s group in Sheffield, UK, where she studied the role of Parkinson’s Disease (PD)-related proteins PINK1 and Parkin in mitochondrial dynamic and mitophagy, using Drosophila Melanogaster as a neurodegenerative disease model as well as fibroblast cells from PD patients. In this work, she unrevealed the biochemical link between PINK1/Parkin pathway and mitochondrial pro-fusion protein Mitofusin (MFN). In December 2010 Dr Ziviani was awarded with both EMBO long term and Marie Curie Action fellowships. Since 2014 she became independent PI c/o department of Biology at the University of Padova where. Ziviani's lab is interested in the molecular pathway leading to neurodegeneration specifically in the context of PD and mitochondria dysfunction. Mitochondrial dysfunction has become a central theme in neurodegenerative diseases, in particular PD. However more work is required to bring mitochondria forward as a therapeutic target in PD. We postulate that while mitochondria communicate with other organelles, impairments of these interorganellar interactions (particularly ER-mitochondria crosstalk) are pivotal for PD onset and progression.

Mitochondrial dysfunction has become a central theme in neurodegenerative diseases, in particular Parkinson’s Disease (PD). NF-kB factors are cardinal transcriptional regulators of inflammation and apoptosis and have been involved in the brain programming of systemic aging as well as in the pathogenesis of several neurodegenerative diseases, including PD. In particular, mice deficient for the c-Rel subunit develop with aging a L-DOPA-responsive parkinsonism associated with loss of dopaminergic (DA) neurons in the substantia nigra, neuroinflammation and accumulation of alpha-synuclein and iron. Parkin, a PD gene and an E3 ubiquitin ligase that regulates mitochondria quality control, upregulates the mitochondrial fusion protein OPA1 through linear ubiquitination of NF-kB essential modulator (NEMO), which is pivotal for the activation of canonical NF-kB pathway. Relevantly, patients with two close OPA1 missense mutations (p.G488R, p.A495V) leading to age-dependent syndromic parkinsonism and dementia have been reported, substantiating a role for OPA1 dysfunction in DA neurons pathology, which is further sustained by the evidence that moderate overexpression of OPA1 is beneficial in primary mitochondrial disease mice model with respectively complex I and IV deficiency. Considering the described scenario, this project hypothesizes that normalizing OPA1 expression levels ameliorates the parkinsonism associated with c-rel/NF-kB deficient mouse. Should impaired OPA1 expression affect mitochondria function in c-rel/NF-kB deficient mice, we expect that normalizing OPA1 levels will contribute to ameliorate the PD phenotypes associated with c-rel/NF-kB mouse, presumably by increasing mitochondrial respiratory efficiency, blunting cytochrome c release and reactive oxygen species production, and exerting cell protection from death. This study will ultimately clarify the role of OPA1 as a crossroad of the above described pathways regulating mitochondrial function, and it will contribute to bring mitochondria forward as a therapeutic target in PD.