bring this page
with you
Structure Department of Biology
Telephone 0498276237
Qualification Professore associato confermato
Scientific sector BIO/10 - BIOCHEMISTRY
University telephone book  Show

Office hours
Dipartimento di Biologia, Complesso Vallisneri, sesto piano NORD, lab numero 59 RIceve previo appuntamento al 045 827 6237
(updated on 26/04/2018 17:09)

Proposals for thesis
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.

Curriculum Vitae
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

Lecturer's Curriculum (PDF): 5F88B05583CFF644D1B8EE2DD21E6CC5.pdf

Research areas
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.

Selected Peer-reviewed Publications
Research Articles
1. Mitochondrial quality control beyond PINK1/Parkin.
von Stockum S, Marchesan E, Ziviani E.
Oncotarget. 2018 9:12550-12551.
2. Postranslational modification of Parkin.
Chakraborty J., Basso V. and Ziviani E.
Biology Direct. Accepted. (2017)
3. The organelle replication connection
Ziviani E. and Scorrano L.
Nature. 538:326-327. (2016)
4. Mitochondrial dynamics and mitophagy in Parkinson's disease: A fly point of view.
Stockum S, Nardin A, Schrepfer E, Ziviani E.
Neurobiol Dis. 90:58-67. (2016)
5. Counteracting PINK/Parkin deficiency in the activation of mitophagy: a potential therapeutic intervention for Parkinson's Disease.
Nardin A, Schrepfer E, Ziviani E.
Curr Neuropharmacol. 14:250-9. (2016)
6. Parkinsonian toxin-induced oxidative stress inhibits basal autophagy in astrocytes via NQO2/quinone oxidoreductase 2: Implications for neuroprotection.
Janda E, Lascala A, Carresi C, Parafati M, Aprigliano S, Russo V, Savoia C, Ziviani E, Musolino V, Morani F, Isidoro C, Mollace V.
Autophagy. 11:1063-80 (2015)
7. Genome-wide RNAi screen identifies the Parkinson disease GWAS risk locus SREBF1 as a regulator of mitophagy.
Ivatt RM, Sanchez-Martinez A, Godena VK, Brown S, Ziviani E, Whitworth AJ.
Proc Natl Acad Sci U S A. 111:8494-9. (2014)
8. Reduction of endoplasmic reticulum stress attenuates the defects caused by Drosophila mitofusin depletion.
Debattisti V, Pendin D, Ziviani E, Daga A, Scorrano L.
J Cell Biol. 204:303-12. (2014)
9. In Epiepsy, BAD is not really bad.
Ziviani E and Scorrano L
Neuron. 74:600-2. (2012)
10. Ryanodine receptor-2 upregulation and nicotine-mediated plasticity.
Ziviani E, Lippi G, Bano D, Munarriz E, Guiducci S, Zoli M, Young KW, Nicotera P.
EMBO J. 30:194-204. (2011)
11. Analysing the role of the PINK1/Parkin pathway in Mitophagy
Rachael I, Ziviani E and Whitworth AJ.
Journal of Neurogenetic. 24: 57-57. (2010)
12. How could Parkin-mediated ubiquitination of mitofusin promote mitophagy?
Autophagy. 6:660-2. (2010)
13. Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin
Ziviani E, Tao RN, Whitworth AJ.
Proc Natl Acad Sci U S A. 107:5018-23. (2010)
14. Modulation of mitochondrial function and morphology by interaction of Omi/HtrA2 with the mitochondrial fusion factor OPA1
Kira M. Holmström, Nicole Kieper, Dalila Ciceri, Fabienne C. Fiesel, Ziviani E, Alexander J. Whitworth, Hartwig Wolburg, L. Miguel Martins, Philipp J. Kahle, Rejko Krüger
Exp Cell Res. 316:1213-24. (2010)
15. Rapamycin activation of 4E-BP prevents parkinsonian dopaminergic neuron loss
Tain LS, Mortiboys H, Ziviani E, Tao RN, Bandmann O, Whitworth AJ.
Nat Neurosci. 12:1129-35. (2009)
16. The plasma membrane Na+/Ca2+ exchanger is cleaved by distinct protease families in neuronal cell death.
Bano D, Munarriz E, Chen HL, Ziviani E, Lippi G, Young KW, Nicotera P.
Ann N Y Acad Sci. 1099:451-5. (2007)

Lecturer's Publications (PDF): 5F88B05583CFF644D1B8EE2DD21E6CC5.pdf

List of taught course units in A.Y. 2019/20
Degree course code (?) Degree course track Course unit code Course unit name Credits Year Period Lang. Teacher in charge
»   SCP4067772 6 1st Year (2019/20) Second
»   SCP4067771 7 1st Year (2019/20) Second
»   SCP4067772 6 1st Year (2019/20) Second
»   SCP4067771 7 1st Year (2019/20) Second
SC1161 COMMON SCN1031971 8 1st Year (2019/20) Annual ITA ELENA ZIVIANI