Assistant Professor, Department of Neurology
My training in axon degeneration began when I was recruited by Dr. Michael Coleman in Cambridge, UK, where I graduated in 2011 with a PhD in Molecular Biology. My graduate studies contributed to elucidating the mechanisms of action of the WldS protein, which confers a strong delay of axon degeneration after neuronal injury. I then joined the laboratory of Prof. Aaron DiAntonio at Washington University School of Medicine, St. Louis, MO, for postdoctoral training. During this time, I discovered a novel pathway regulating axon survival, mediated by the E3 ubiquitin ligase Phr1, in mouse models of acute nerve injury. In 2014, I was recruited to the University at Buffalo, where I shifted my focus from an axon-centric view of degeneration to a comprehensive understanding of the cellular mechanisms during nerve damage. I relocated to the Ohio State University Wexner Medical Center in 2022 to establish a research program that addresses the interaction between glia and axons during aging and disease. My past and current funding reflects that my research is applicable to a wide spectrum of neurodegenerative conditions (Alzheimer’s Research Trust, Muscular Dystrophy Association, American-Italian cancer foundation, Guillain-Barre Syndrome |CIDP Foundation, NINDS R01).
Research Interests
Axon degeneration causes the overt symptoms of many neurodegenerative diseases and conditions. I am highly motivated to unveil the driving forces of axon degeneration and act on these forces to alter the rate of axon loss. My science uses a combination of various in vitro and in vivo molecular, biochemical, and pharmacological approaches in murine models of axonal demise. I recently discovered that Schwann cells regulate the resistance of injured axons to degeneration through changes in their energy metabolism (Nature Neuroscience, PMID: 32807950). This finding introduces a fundamental paradigm shift for the understanding of axon degeneration, which most neuroscientists believe is exclusively regulated by cell-autonomous mechanisms. As the landscape of the signaling events after axon injury is being characterized, I continue to work towards the goal of elucidating the mechanism of axon loss, with the final aim to relate the future findings in the laboratory mouse to acute injuries in patients and to real-life chronic degeneration.
Publications
Education
- 2011 – 2014:Postdoctoral Research Scholar, Washington University School of Medicine in St. Louis, MO
- 2006 – 2011: Ph.D. Neuroscience. University of Cambridge, Cambridge, UK
- 2004 – 2005: Specialization, Pharmacological Research. Mario Negri Institute, Milan, Italy
- 2004: M.Sc. Medical Biotechnology, University of Milan, Italy
- 2004: B.S. Medical Biotechnology, University of Milan, Italy
Editorial Boards
- Frontiers in Neurology
Other Editorial Activities
- Volume Editor: “Axon degeneration: Methods and Protocols”, Methods in Molecular Biology series, Volume 2143, Springer.
Professional Activities
- ECR NIH/NINDS member, Neural Oxidative Metabolism, Mitochondria and Cell Death study section
Honors and Awards
- 2021 Women in Science Travel (WIST) Fund COVID-19 Relief award
- 2018 GBS|CIDP foundation research grant
- 2014 MDA Career Development Award
- 2012 Travel award, Fine Science award
- 2011 American Italian Cancer Foundation Postdoctoral Fellow
- 2009 SfN Graduate Travel award
- 2008 Queens’ College international travel award
- 2006 Alzheimer’s Research Trust Scholar and MRC Studentship award
- 2006 Alzheimer’s Research Trust National Meeting travel award
- 2004 “Regione Lombardia” Fellowship for Pharmacological Research Specialist studies
Advisory and Consulting
- Scientific advisory member of the Charcot-Marie-Tooth Research Foundation
Grants and Projects
- 2021 – 2026: National Institute of Health R01NS123450-01 Role: PI
Title: Energizing and Protecting Axons Through Metabolic Coupling to Schwann Cells - 2020 – 2024: National Institute of Health R01NS111024 Role: Co-I
Title: Elucidating the trophic support of long axons by metabolic signaling in oligodendrocytes