Leonidas Stefanis

Dr. Stefanis obtained his MD from the National and Kapodistrian University of Athens (NKUA) Medical School in 1987 and his PhD from the same University in 1992, with work related to the molecular basis of thalassemia. In 1991, he moved to the US, where he trained as Resident in Neurology at Columbia University in New York. In 1995, he embarked on a post-doctoral fellowship in the laboratory of Dr. Lloyd Greene, in the Dept. of Pathology, while in parallel he completed a two-year fellowship on Neurobehaviour, in the Dept. of Neurology at Columbia University. His work during this time centered on mechanisms of neuronal cell death. In 1998 he was appointed Assistant Professor of Neurology in the Center for Neurodegenerative Diseases in the Dept. of Neurology at Columbia University, position which he held up till 2003. During this time, he focused on the pathogenesis of neurodegenerative disorders, with an emphasis on Parkinson’s Disease (PD).

In 2003 he moved back to Greece as Researcher Level B at the Biomedical Research Foundation of the Academy of Athens (BRFAA), and set up a laboratory focusing on mechanisms of neurodegeneration, in particular in relation to protein degradation systems, alpha-synuclein and PD. In 2006 he was appointed Associate Professor in the NKUA Medical School, while he continued his work at BRFAA as affiliated investigator. In 2011 he was appointed Director of the Second Department of Neurology at Attikon Hospital and in 2012 he was elected to the position of Professor of Neurology and Neurobiology at the NKUA. In 2017, he moved as Director to the First Department of Neurology at Eginitio Hospital. Currently, he is investigating various areas of PD pathogenesis, ranging from the bench to the bedside. He is examining the genetic underpinnings of the disease in the Greek population. A special focus is rare cases with genetic synucleinopathies, carriers of the p.A30G or p.A53T SNCA mutations, as well as patients with GBA1 or PRKN mutations.

He is examining the utility of using alpha-synuclein, elements of the Autophagy Lysosome Pathway (ALP), or measurements of PRKN expression as disease biomarkers. He is examining pathways of neurotoxicity and aggregation induced by aberrant alpha-synuclein, with an emphasis on the involvement of protein degradation pathways, such as Chaperone-Mediated Autophagy. Conversely, he applies experimental therapeutics aiming to boost such intrinsic pathways, in order to confer neuroprotection in synucleinopathies. He is using a wide array of approaches, ranging from cellular and animal models to studies of patients’ biological material.