Gruppo guidato da Elena Tamagno
Tel +39 011 6707763 - 6604
Fax +39 011 6707753
Born in Turin, on July 14, 1967. Italian
Education and training
1986 Graduate from High School
1986-1990 University Degree in Biological Science, University of Turin, Italy
1990 Professional qualification, University of Turin
1990-1994 Specialization Degree on Clinical Pathology, University of Turin
1995-1998 PhD in Hepatological Sciences, University of Modena
1998-2003 Graduate Technician, Dept. Experimental Medicine and Oncology, General Pathology Section, University of Turin
2004-2016 Assistant Professor of the Faculty of Medicine and Surgery, University of Turin
2017-2021 Associate Professor of General Pathology, of the Faculty of Medicine and Surgery, University of Turin
2022-today Full Professor of General Pathology, of the Faculty of Medicine and Surgery, University of Turin
Società Italiana di Patologia (Italian Society of Pathology)
Society of Free Radical Research
In her scientific activity Elena Tamagno has been involved in the study of the pathogenetic role of oxidative stress in the pathogenesis of different diseases. Recently her attention has been focused on the relationship between oxidative stress and amyloidogenic processing of amyloid beta precursor protein (APP). In her recently publications it has been proposed a sequence of events linking oxidative stress, induction of BACE1, the rate-limiting enzyme for Abeta production, and apoptotic cell death.
1990-1992 Study on hepatotoxicity mediated by halogenated pro-oxidant compounds performed with Prof. Oliviero Danni, Department of Experimental Medicine and Oncology, General Pathology Section, University of Turin.
1992-1993 Study on effects mediated by androgens and estrogens on the growth of chemical-induced rat mammary carcinomas, performed with Prof. Oliviero Danni, Department of Experimental Medicine and Oncology, General Pathology Section, University of Turin.
1993-1995 Study on hepatotoxicity of ethanol in different “in vivo” and “ex vivo” models: role of acetaldehyde, performed in collaboration with Prof. Giuseppe Poli, University of Turin.
1995-1997 Study on antioxidant properties of the physiologic steroid, dehydroepiandrosterone in different cellular models such as hepatic and brain microsomes as well oxidized low density lipoproteins, performed in collaboration with Prof. Emanuele Albano and Prof. Giorgio Bellomo, Università del Piemonte Orientale.
1997-2000 Pathogenesis of diabetes mellitus: modulation of oxidative stress mediated complications using antioxidant compound such as dehydroepiandrosterone in different cellular models, performed in collaboration with Prof. Giuseppe Boccuzzi, Dept. Endocrinology, University of Turin.
2000-2002 Pathogenesis of Alzheimer’s disease; study on the role of oxidative stress on the BACE1 over-expression, performed in collaboration with Prof. Massimo Tabaton, Dept. Neuroscience, University of Genoa; Prof. George Perry and Prof. Mark Smith, Case Western Reserve University, Cleveland, OH.
2002-2003 Pathogenesis of Alzheimer’s disease: study of signalling events involved in amyloid beta-induced, oxidative stress dependent, neuronal apoptosis, performed in collaboration with Prof. Massimo Tabaton, Dept. Neuroscience University of Genoa.
2004-today Pathogenesis of Alzheimer’s disease: Study of the molecular mechanisms underlying the up-regulation of BACE1, performed in collaboration with Prof. Massimo Tabaton, Dept. Neuroscience, University of Genoa.
Our spinoff provides scientific expertise, animal models, equipment and facilities to pharmaceutical, biotechnology, and medical device Companies and to Research Centers for proof–of-concept or pilot in vivo studies.
Individuato nell’autofagia uno dei meccanismi responsabili della neurodegenerazione nell’atrofia muscolare spinale. Su Cell Death and Disease (gruppo Nature) i risultati di un team di ricerca internazionale guidato dal nostro direttore Alessandro Vercelli.
Scopri e sostieni i nostri progetti: ricerca di base e applicata insieme per prevenire e combattere gli effetti dell'invecchiamento.
La pubblicazione su Autophagy. I nostri ricercatori hanno chiarito uno dei meccanismi che impedendo alle cellule del cervello di 'ripulirsi' favorisce lo sviluppo dell'Alzheimer, la più comune patologia legata all'invecchiamento.