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.
MAJOR ACHIEVEMENTS & PUBLICATIONS
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