Professor Colin Masters is a native of Perth, Western Australia, and  did his undergraduate and postgraduate training in medicine and in medical science at the University of Western Australia. He is currently Professor of Pathology in the University of Melbourne and Consultant, Chief of the Neuropathology Laboratory, and Chair of the Senior Scientists Council at the Mental Health Research Institute in Victoria.

He is a Fellow of the Royal College of Pathologists, the Royal College of Pathologists of Australasia, the Australian Academy of Science and the Australian Academy of Brain Sciences.  He has published 350 papers cited by PubMed, and has received numerous prestigious awards for his achievements.

 

The outstanding achievement of the last 3 decades in the field of degenerative diseases of the central nervous system has been the clear demonstration that Alzheimer's disease is a direct consequence of the accumulation, deposition or over-expression of beta amyloid peptides derived from the beta-amyloid precursor protein. It was a conclusion reached after years of fierce controversy, and Professor Colin Masters was instrumental, along with his collaborators, in making many of the pioneering findings that implicated beta amyloid peptides as the causative agent in Alzheimer's disease.

 

Professor Masters' work on Alzheimer's disease and Creutzfeldt-Jakob disease began in the 1970s, and in the 1980s he published a series of seminal papers which described peptides and proteins from the neuropathological lesions (plaques) found in the brains of Alzheimer's disease patients; these studies of post-mortem material led to the identification of beta-amyloid peptides. This work and many of the important papers that followed was done in close collaboration with Professor Konrad Beyreuther in Germany.

 

They played a central role in the development of the amyloid hypothesis by cloning the gene for and the sequencing amyloid precursor protein itself the protein that gives rise to the self aggregating peptides that combine to produce the characteristic neuropathological lesions of Alzheimer's disease. They then played a major role in the identification of the pathways that lead to the accumulation and toxicity of these molecules in the aging brain; they also provided the first evidence that heavy metals and oxidative stress might act as predisposing factors for amyloidosis.  These were key contributions to the understanding not only of the generation, aggregation and turnover of the aberrant peptides, but also of their toxic consequences. To his credit he promulgated and defended the centrality of the beta-amyloid peptides during difficult years against influential and vocal proponents of other proposals. Professor Masters also made fundamental contributions to the neuropathology and a etiology of prion encephalopathies and notably of CJD and familial forms of the spongiform encephalopathies.

 

Professor Masters has been particularly interested in the potential drug-targets in this system, some aimed at facilitating the release of these toxic peptides from neurons, and others directed towards the toxicity and aggregation of these peptides.  He has sought to collaborate with biotechnology and pharmaceutical industry partners to identify molecules that could inhibit the formation or deposition of beta-amyloid. Examples include metal chelators that inhibit aggregation, and protease inhibitors that inhibit the formation of beta-amyloid formation have been found. The current therapeutic approaches are based on this understanding of the molecular pathology of the disease, although as yet there are no clinical data to show whether these initiatives will have any therapeutic efficacy. We are in a period of rapid advancement in this field, which is generally regarded the greatest challenge in the field of neuropathology. Although there is still a long way to go before all of the mechanisms that contribute to this pathology are completely clarified, great progress has been made in reaching this goal, and there is great hope for therapeutic achievements in the future. 

Professor Colin Masters is an outstanding figure in the development of this field, and we seek to congratulate him on his achievements.

 

Overall, the purpose of Prof Masters' contributions in the work around the diseases caused by proteins which aggregate in the adult human brain has been vindicated by a rich variety of discoveries which have had a wide impact in understanding the normal and abnormal functions of the ageing brain and have opened a strategy for rational therapeutic intervention.

 

In conclusion, Professor Colin Masters has been an outstanding clinician, educator and researching scientist with his unrivalled contributions of the understanding the normal and abnormal functions of the ageing brain and have opened a strategy for rational therapeutic intervention. He was instrumental in discovering the role of amyloid pathoetiological process that leads to neuronal attrition in Alzheimer's Dementia. He very much deserves to be the 4th recipient of the Grand Harridan International Award 2005-2006.