Michael Hayden
MB, ChB, PhD, FRCP (C), FRSC, C.M., O.B.C.
Professor, Department of Medical Genetics, Faculty of Medicine, UBC
University Killam Professor
Full Member
Dr. Hayden is a Killam Professor at the University of British Columbia, the highest honour UBC can confer on any faculty member. Dr. Hayden was named one of the 50 Canadians born in the 20th century who have changed the world. He is the co-founder of five biotechnology companies and currently sits on different public and private boards of biotechnologies companies. Author of over 950 peer-reviewed publications, Dr. Hayden’s research focuses on translational medicine, including Huntington Disease, predictive, personalized medicine, drug development and lipoprotein disorders. His research group identified the first mutations underlying Lipoprotein Lipase (LPL) Deficiency and developed gene therapy approaches to treat this condition resulting in the first approved gene therapy product (Glybera) in a major market. Dr. Hayden is the most cited author in the world on ABCA1 and Huntington Disease. Dr. Hayden is the recipient of numerous prestigious honours and awards. Most recently, he was awarded the degree of Doctor of Science in Medicine (honoris causa), UCT (2024) and the 2023 Lifetime Achievement Award by the Huntington Study Group, USA. In 2017, Dr. Hayden was inducted into the Canadian Medical Hall of Fame. In addition to mentoring over 100 graduate students and postdocs, Dr. Hayden is also a TED mentor.
Contact Info
950 W 28th Ave.
Vancouver, BC V5Z 4H4
Research Information
Dr. Hayden’s work focuses on understanding the genetic roots of illness and using that understanding to develop better approaches to treatment for patients. His research focus is primarily on genetic diseases, including gene therapy, Huntington disease, predictive and personalized medicine and drug development. Huntington Disease (HD) is a devastating incurable neurodegenerative disease that affects about 5,000 Canadians. Inheriting a single mutant copy of the Huntingtin (HTT) gene from either parent is sufficient to cause HD. The mutated HTT gene codes for production of the toxic, mutant huntingtin protein (mHTT) that is responsible for killing brain cells in HD. Importantly, the other, non-mutated (or normal) copy of the huntingtin protein is critical for the health of brain cells. Consequently, Dr. Hayden’s research goals are to reduce mHTT through multipronged approaches that specifically target the mutant gene and also develop approaches to enhance the clearance of mutant protein. The ultimate goal of Dr. Hayden’s research is to develop new therapies that slow down or reverse progression of HD and lead to preventative therapy for pre-symptomatic individuals.
PublicationsKeywords
- Huntington disease
- drug development
- gene therapy
- genetics
- biomarkers
- neurodegenerative diseases