Email: ted.fon [at] mcgill.ca (Edward Fon)
Website: Fon Lab
Recent Publications: PubMed
Academic Affiliations: Neurology and Neurosurgery
Clinical Interests: Parkinson's, movement disorders
Research Groups: Neurodegenerative Diseases, Neuroimaging and Neuroinformatics
Dr. Edward Fon is a full Professor in the Department of Neurology and Neurosurgery at McGill University and the Scientific Director of the Montreal Neurological Institute. He is a clinician-scientist at the Neuro where he practices in the area of Parkinson’s disease and movement disorders. He serves as Director of the McGill National Parkinson Foundation Centre of Excellence and of the FRQS Quebec Parkinson Network.
Dr. Fon obtained his M.D. from the Université de Montréal in 1989 and then completed his Neurology Residency as well as a Clinical and Research Fellowship in Neurogenetics at McGill University. He joined the MNI in 1999 after four years as a post-doctoral research fellow at the University of California, San Francisco, where he conducted genetic studies leading to a breakthrough in the understanding of dopamine transmission.
Dr. Fon's research focusses on the molecular events leading to the degeneration of dopamine neurons in Parkinson's disease. He is particularly interested in α-Synuclein, parkin and PINK1, all genes known to cause familial forms of the disease. His work developing cellular models of Parkinson’s disease using patient-derived induced pluripotent stem cells (iPSCs) could provide important clues about the mechanisms of dopamine neuron death and lead to innovative therapeutic strategies for the disease. Dr. Fon’s many awards include the CIHR Clinician-scientist award, the Prix de Jeune Chercheur Blaise Pascal, the EJLB Foundation Scholar Research Award, and a National Scholar Award from the Fonds de la Recherche en Santé du Québec. He is a former Killam Scholar at the MNI. In 2015, he was elected member of the American Society for Clinical Investigation (ASCI).
Tang MY, Vranas M, Krahn A, Pundlik S, Trempe JF, Fon EA. Structure-guided mutagenesis reveals a hierarchical mechanism of Parkin activation. Nat. Commun. 2017; 8:14697. doi: 10.1038/ncomms14697
McLelland GL, Lee SA, McBride HM, Fon EA. Syntaxin-17 delivers PINK1/parkin-dependent mitochondrial vesicles to the endolysosomal system. J. Cell Biol. 2016; 214(3):275-91
Durcan TM, Fon EA. The three P’s of Mitophagy: PARKIN, PINK1 and Post-Translational Modifications. Genes Dev. 2015; 29(10):989-999
Koyano F, Okatsu K, Kosako H, Tamura Y, Go E, Kimura M, Kimura Y, Tsuchiya H, Yoshihara H, Hirokawa T, Endo T, Fon EA, Trempe JF, Saeki Y, Tanaka K, Matsuda N. Ubiquitin is phosphorylated by PINK1 to activate parkin. Nature. 2014; 510(7503):162-6
Durcan TM, Tang MY, Pérusse JR, Dashti EA, Aguileta MA, McLelland GL, Gros P, Shaler TA, Faubert D, Coulombe B, Fon EA. USP8 Regulates Mitophagy by Removing K6-linked Ubiquitin Conjugates from Parkin. EMBO J. 2014; 33(21):2473-91
Trempe J-F, Sauvé, V, Grenier K, Seirafi, M, Tang MY, Ménade M, Krett J, Wong K, Kozlov G, Nagar B, Fon EA, Gehring K. Structure of parkin reveals mechanism of ubiquitin ligase activation. Science. 2013; 340(6139):1451-5