Michael Hayden

Professor

Research Classification

Genetic Diseases
Neurodegenerative Diseases

Research Interests

Huntington disease
Disease progression
Diabetes

Relevant Degree Programs

 

Biography

Dr. Michael Hayden is a Killam Professor at the University of British Columbia (UBC) and holds the Canada Research Chair in Human Genetics and Molecular Medicine. He is a Senior Scientist at the Center for Molecular Medicine and Therapeutics (CMMT) in Vancouver, Canada; a genetic research center within UBC. He is also the Program Director of the Translational Laboratory in Genetic Medicine in Singapore, and was appointed in 2012 as the President of Global R&D and Chief Scientific Officer at Teva Pharmaceutical Industries.

Dr. Hayden was recently named one of the 50 Canadians born in the 20th century who have changed the world. Dr. Hayden is the co-founder of three biotechnology companies: NeuroVir Therapeutics Inc., Xenon Pharmaceuticals Inc., and Aspreva Pharmaceuticals Corp. Dr. Hayden sits on different public and private boards including Xenon Pharmaceuticals and Lycera.

Author of over 860 peer-reviewed publications and invited submissions (h-index 135 Google Scholar;112 Web of Science), Michael has focused his research primarily on genetic diseases, including genetics of diabetes, lipoprotein disorders, Huntington disease, predictive and personalized medicine. Michael and his research group have identified 10 disease-causing genes which includes the identification of the major gene underlying high-density lipoprotein (HDL) in humans. This gene, known as ABCA1, has major implications for atherosclerosis and diabetes. Michael also identified the first mutations underlying Lipoprotein Lipase (LPL) Deficiency and developed gene therapy approaches to treat this condition, resulting in the first approval of gene therapy in the world in 2012 (Glybera). He is the most cited author in the world for ABCA1 and Huntington Disease.

Michael is the recipient of numerous prestigious honours and awards. He was recently inducted into the Canadian Medical Hall of Fame (2017). He was named one of PharmaVoice’s “100 of the Most Inspiring People” (2015); awarded an Honorary Doctor of Science by the University of Gottingen (2014); awarded the Luminary award by the Personalized Medicine World Conference (2014); awarded the Diamond Jubilee Medal, on behalf of HRH Queen Elisabeth II (2012), in recognition of his significant contributions and achievements; received the Margolese National Brain Disorder Prize (2011), awarded to Canadians who have made outstanding contributions to the treatment, amelioration, or cure of brain diseases; awarded the Killam Prize by the Canada Council of the Arts (2011), in recognition of his outstanding career achievements; and the Canada Gairdner Wightman award (2011), recognizing him as a physician-scientist who has demonstrated outstanding leadership in medicine and medical science. Michael has also been awarded the Order of Canada (2011), and the Order of British Columbia (2010). He was named Canada’s Health Researcher of the Year by CIHR (NIH of Canada) in 2008, and he received the Prix Galien in 2007, which recognizes the outstanding contribution of a researcher to Canadian pharmaceutical research. In. Michael is committed to empowering others.

In addition to mentoring over 100 graduate students and postdocs, he is also a TED mentor. Michael has initiated and leads an international effort to bring benefit to a community living with HIV/AIDS in South Africa. In collaboration with colleagues around the world, he spearheaded and built a youth-friendly recreation, counseling, and Learning Centre in direct partnership with the township of Masiphumelele in Cape Town.

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Postdoctoral Fellows
Any time / year round

Hayden Lab Research Projects
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, our 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.

My current research projects include:
Silencing the gene that causes Huntington disease– Mutant huntingtin protein is the cause of Huntington disease (HD) and engages in a variety of aberrant interactions in neurons. Preventing generation of this toxic protein by gene silencing, the process of switching off a gene, should prevent all subsequent pathology and prevent or delay the onset of HD. Everyone has two copies of the huntingtin gene. In HD, one of these copies carries the mutation while the other copy is normal. The normal huntingtin protein is important for maintaining neuronal health and long-term reduction of this protein may not be well-tolerated. We are developing a strategy of silencing only the mutant copy of a patient’s huntingtin gene using antisense oligonucleotides targeted to HD mutation-associated single nucleotide variants as a treatment for HD.
Modulating mHTT post-translational modifications (PTMs) to enhance its clearance – Huntingtin (HTT) undergoes a myriad of post-translational modifications (PTMs) including phosphorylation, proteolytic cleavages and fatty acylation that influence the protein function, localization and clearance. Those PTMs are essential for neuronal viability, but are altered in HD. We have shown that promoting or preventing specific HTT PTMs can either dramatically improve or exacerbate HD symptoms. There is also evidence that HTT PTMs work in concert and may regulate one another. However, the interactions between the networks of HTT PTMs remain mostly unstudied. Our objectives are therefore to identify new rate-limiting PTMs, characterize the interrelationship of the HTT PTM network in vivo and understand how it relates to HTT function, stability and clearance. This project will allow us to determine and validate molecular targets for therapeutic strategies that could be used in synergy with HTT gene silencing.
Discovery of novel therapeutic targets for neuroprotection in Huntington Disease – Glutamate excitotoxicity and mitochondrial dysfunction are critical, closely-linked pathogenic mechanisms in several acute and neurodegenerative brain disorders, including HD. Together, these processes contribute to altered intracellular calcium dynamics, bioenergetic defects, cell death signaling, and synaptic instability. We are investigating novel therapeutic targets involved in these pathways with the goal of improving mitochondrial health and normalizing synaptic function in HD.

Population genetics and epidemiology of the Huntington disease mutation – The HD mutation is associated with specific sets of genetic variants in the surrounding HTT gene, known as haplotypes. We are performing detailed investigations of haplotypes HD mutation in different populations around the world. Haplotypes of the HD mutation allow for identification of new targets for therapeutic gene silencing and offer insight into the origin of the HD mutation in different ethnic groups. We additionally study how many people have the HD mutation, how often this mutation results in HD symptoms, and how often unstable new mutations for HD occur in the general population.

I support public scholarship, e.g. through the Public Scholars Initiative, and am available to supervise students and Postdocs interested in collaborating with external partners as part of their research.
I support experiential learning experiences, such as internships and work placements, for my graduate students and Postdocs.
I am open to hosting Visiting International Research Students (non-degree, up to 12 months).

Publications

 
 

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