Previous Samuel Gershon Medal Recipients
The 2015 recipient of the Samuel Gershon Medal for Lifetime Achievement in Translational Neuroscience
Professor Colin Masters
B Med Sci (Hons), MBBS, MD, Hon.DLitt W.Aust., FRCPath, FRCPA, FAA, FTSE
Professor Masters is currently the Executive Director of the Mental Health Research Institute, and a Laureate Professor at the University of Melbourne. He is also the Senior Deputy Director of the Florey Institute of Neuroscience and Mental Health, and a consultant at the Royal Melbourne Hospital. His achievements have been recognised by the receipt of many international awards.
Colin Masters has focused his career on research in Alzheimer's disease and other neurodegenerative diseases, including Creutzfeldt-Jakob disease. His work over the last 35 years is widely acknowledged as having had a major influence on Alzheimer’s disease research world-wide, leading to the continued development of diagnostics and therapeutic strategies.
Career: He began his research career as a 1966 summer student working with Evan Morgan (Physiology, The University of Western Australia) on the placental transfer of plasma proteins. His interests in neuroscience stem from when he then took the opportunity to pursue a Bachelor of Medical Science degree with Brian Johnstone and Judith Laszlo, resulting in the first demonstration of brain-stem evoked responses to auditory stimuli in humans. By the end 1967, he began ongoing study of the transmissible spongiform encephalopathies (prion diseases) and then ventured into the epidemiology of Creutzfeldt-Jakob disease, the familial patterns of these diseases, and the identification of a special subgroup (the Gerstmann-Sträussler syndrome [GSS]) in which abundant amyloid deposition is a hallmark. In 1978 Masters began to study the nature of the amyloid deposits found in the brain in Alzheimer’s disease (AD) and a collaboration was formed in 1984 between Masters and Konrad Beyreuther (then at the Institute of Genetics, Cologne). Together they uncovered the N-terminal sequence of the Alzheimer plaque amyloid, at the same time as the N-terminal sequence of vascular amyloid was determined by George Glenner (with whom Masters had also collaborated).
In 1989 he moved to the University of Melbourne and his research evolved into developing therapeutic strategies based around the central amyloidogenic pathway in AD. As the real potential for development of pharmaceuticals that could delay the onset or slow progresssion of AD became apparent, Masters initiated collaborations with major pharmaceutical companies SmithKline Beecham and Merck. Those collaborative studies have been brought to a point where Phase 3 clinical trials are in progress.
Masters and colleagues then developed a parallel strategy around studies of the toxic gain-of-function of Aβ amyloid as it accumulates in the brain and he and his research group have identified compounds that prevent Cu2+ interacting with Aβ, and have the additional desirable properties of abrogating the generation of H2O2 and simultaneously cause solubilisation of polymerised Aβ. Such compounds have been tested in experimental models of AD with positive results. Two compounds have been trialled in Phase 2a studies in humans with mild to moderate AD. If confirmed in larger (Phase 2b/3) studies, this may become one of the first pharmacological interventions to test the Aβ theory of AD.
With the emergence of variant forms of CJD as a major threat to public health, Masters re-established a research group on prion dementias. He brought the knowledge gained from his AD studies, particularly with respect to the roles of metal ions, to bear on the problem of PrP toxic gain-of-function. This may also lead to new approaches to therapy for the prion dementias, for which there are no effective treatments at present.
In summary, Masters’ career has come full circle, from the pathological study of human brain disease to clinical trials, and from discovery and characterisation of the Aβ aggregation in AD, to the development of a coherent theory on the mechanisms of Aβ amyloid production and its role in causation of neurodegeneration. This theory has become the generally accepted paradigm for investigating Alzheimer disease. The single, most characteristic, feature of Masters’ research has been the way in which he has approached gene and protein structure and function for a variety of diseases caused by proteins that aggregate in the adult human brain. He has used the resulting data to generate a rich variety of discoveries that have had a wide impact in understanding normal and abnormal brain function in disease and in ageing. In the best traditions of translational research, Masters has continued to identify and develop effective rational therapeutic and diagnostic strategies for disease modification, perhaps even prevention.
His publication record is impressive with a total of 897 as of April, 2015. The impact of his publications is reflected in his h-index 121 in Google Scholar from of 66,111 total citations) and 106 in ISI-Thomson Scientific (from 49,324 total citations).
His work over the last 35 years is has had a major influence on Alzheimer’s disease and Creutzfeldt-Jakob disease research world-wide making him an incredibly worthy recipient of the 2015 Samuel Gershon Medal for Lifetime Achievement in Translational Neuroscience.
The 2014 recipient of the Samuel Gershon Medal for Lifetime Achievement in Translational Neuroscience
Professor Samuel Frank Berkovic
AC, MD, FAA, FRACP, FRS
Professor Sam Berkovic is Laureate Professor in the Department of Medicine, University of Melbourne, and Director of the Epilepsy Research Centre at Austin Health. His medical degree (MB BS; 1977) and doctorate (MD) were completed at the University of Melbourne before he undertook a three-year Fellowship at McGill University. He returned to Melbourne in 1987 where he is a practicing neurologist and clinical researcher with a special interest in establishing close research links with basic scientists. Despite early advice that a successful clinical academic had to have a laboratory, he found his niche in clinical research and translation.
His early work was in neuroimaging where he was a pioneer in the application of MRI and single photon emission computed tomography in epilepsy, and especially epilepsy surgery. This work was rapidly applied to routine clinical use and remains so today. In the late 1980s he realized the potential for clinical genetic research in epilepsy, utilizing the NHMRC twin registry and working with large pedigrees. This led, together with molecular genetic collaborators in Adelaide and Germany, to the discovery of the first gene for epilepsy in 1995. Subsequently he and his group have been involved in the discovery of many of the known epilepsy genes. This has changed the conceptualisation of the causes of epilepsy, having a major impact on directions of epilepsy research, and has directly translated to impacting daily clinical diagnosis and counselling, as well as refining treatment. He heads a large Program Grant integrating genetic, imaging and physiological studies in epilepsy. He was elected a Fellow of the Royal Society in 2007 and awarded a Companion of the Order of Australia in 2014.