Garth Cooper

Overview

I was appointed Professor of Discovery and Experimental Medicine and Director of the Centre for Advanced Discovery and Experimental Therapeutics in 2011. I have also had a Chair at the Unversity of Auckland, New Zealand, since 1995.

My research over the last six years has had two closely related aims: firstly, to elucidate the mechanisms of diabetic organ damage; and secondly, to determine the metabolic basis of age-related dementia, starting with Alzheimer''s Disease and Huntington''s Disease; and to use diabetic organ damage (particularly neurodegeneration) as a ''Rosetta Stone'' to find mechanistically relevant perturbations that might be shared among them. This approach is based on epidemiological evidence and molecular data linking diabetes with common age-related dementias.

I was elected a Fellow of the Royal Society of New Zealand in 1998 and a Fellow of the Academy of Medical Sciences in 2013.

Biography

After completing my medical and pathology training in New Zealand, I was awarded a Nuffield Medical Fellowship to study for a doctorate with Ken Reid in the MRC Immunohistochemistry Unit at the University of Oxford, where I discovered and isolated the beta-cell hormone amylin from the pancreatic islets of type-2 diabetes patients. Starting in Oxford and continuing in the USA and back in New Zealand, I characterised the two intertwined structure-activity relationships of amylin as a hormone and as a cytotoxic amyloid-forming protein. In 1987, I founded and was sole scientific founder of Amylin Pharmaceuticals Inc., a biotechnology corporation in San Diego, California, USA. The company, where I was Chief Technical Officer/Executive Board Member until 1992, was set up to progress amylin as a drug lead, which underpinned the development of a new class of anti-diabetic medicines, termed amylin agonists. This ultimately lead to the licencing of pramlintide, the first non-aggregating amylin chimaera, Symlin®, approved by the US Food and Drug Adminsitration for treatment of diabetes in 2005.

In 1993, I returned to New Zealand to become Associate Professor, then Professor at the University of Auckland, where I continued my research into amylin and other peptide hormones, demonstrating, for example, that amylin becomes deficient in both major types of diabetes and that human amylin causes islet beta-cell degeneration via the FAS/FASL/FADD/caspase-8 signalling pathway. In parallel my research has been translated into further new first-in-class therapeutic molecules for the treatment of diabetes: these are the synthetic GLP-1 agonists Byetta® and Bydureon®; and into the discovery of new classes of molecules that suppress amylin-mediated beta-cell death, which also have the potential to be new anti-diabetic agents.

More recently both in Auckland and since my appointment at The University of Manchester, I have shown that defective copper regulation is a substantive pathogenic mechanism causing diabetic organ damage in the heart and kidneys, and have identified severe metabolic perturbations in glucose, sorbitol, fructose, urea, vitamin B5 and copper that potentially cause neurodegeneration in age-related dementias.