Michael R. Hayden

Michael R. Hayden

Genetics has allowed medicine to move beyond treating symptoms and start treating the underlying causes of disease.

"No diseases are hopeless anymore," says Dr. Hayden. "The way I see them is that their secrets have just not yet been identified."

Dr. Hayden’s work focuses on understanding the genetic roots of illness and using that understanding to develop better approaches to treatment for patients. He researches diabetes, coronary artery disease, and is part of a large collaboration to determine the genetic basis for adverse drug reactions in children. Much of his career has also been dedicated to understanding the development of Huntington disease and finding a way to cure it.

"When we started working on Huntington disease, the future was dark and patients and families felt hopeless," says Dr. Hayden. "Today, that has all changed."

Researchers in the Hayden laboratory have found a critical pathway in the development of juvenile forms of Huntington’s disease. Blocking the action of caspase-6 prevents the progression of the disease in mice. This finding could lay the groundwork for an effective approach to therapy for Huntington disease.


Aubrey J. Tingle Prize, Michael Smith Foundation for Health Research – 2011

Killam Prize, Canada Council of the Arts – 2011

Margolese National Prize, University of British Columbia – 2011

Canada Gairdner Wightman, Gairdner Foundation – 2011

Genome BC Award for Scientific Excellence, LifeSciences British Columbia – 2011

Order of Canada – 2010

Order of British Columbia – 2009

Canada's Health Researcher of the Year: Canadian Institutes of Health Research Michael Smith Prize in Biomedical and Clinical Research – 2008

Prix Galien (Canada) – 2007

Ross, CJD, Katzov-Eckert, H, Dubé, MP, Brook, B, Rassekh, SR, Barhdadi, A, Feroz-Zadac, Y, Visscher, H, Brown, AMK, Rogers, PC, Phillips, MS, Carleton, B, Hayden MR. TPMT and COMT genetic variants are predictive for severe hearing loss in children receiving cisplatin chemotherapy. Nat Genet. 2009 41(12):1345-9. PMID:19898482

Graham RK, Deng Y, Slow EJ, Bissada N, Lu G, Pearson J, Betram L, Shehadeh J, Warby SC, Roy So, Wellington CL, Leavitt BR, Raymond LA, Nicholson DW, Hayden MR. Cleavage at the caspase 6 site in huntingtin is required for motor dysfunction, neurodegeneration and excitotoxicity in Huntington Disease. Cell. 2006; 125:1179–1191