Hosted
Sessions 3：Life Sciences
Colin L. Masters
Character introduction
Positions
The Florey Institute, The University of Melbourne (2012- ).
Laureate Professor of Dementia Research, The University of Melbourne (2002- ).
Consultant, The Royal Melbourne Hospital and Melbourne Health (1989- ) and Austin Health (2015).
Tertiary education
1967 B.Med.Sci.(Physiology) (First Class Honours), University of Western Australia.
1970 M.B., B.S., University of Western Australia.
1977 M.D., University of Western Australia.
Honors and awards
Masters has won many prestigious prizes and awards, including the Potamkin Prize of the American Academy of Neurology (1990), the Max Planck Award of the von Humboldt Foundation (1991), the Zülch prize of the Max Planck Society (1995), the Faisal International Prize (1997), the Alzheimer Award from the University of Munich (1998), the Lennox K Black Prize from Thomas Jefferson University (2006), the Grand Hamdan International Award (2006), and the Victoria Prize from the Minister for Innovation, State Government of Victoria and the Smorgon Foundation. In 2008 he was awarded the Honorary Degree of Doctor of Letters from the University of Western Australia. He is active in the Australian Academy of Science (AAS) and the Australian Academy of Technological Sciences and Engineering (AATSE), and continues to lecture widely at undergraduate and postgraduate levels. He has been appointed by the Australian Government as Chair of the National Health Committee, principal committee of the National Health and Medical Research Council of Australia.
The Florey Institute, The University of Melbourne (2012- ).
Laureate Professor of Dementia Research, The University of Melbourne (2002- ).
Consultant, The Royal Melbourne Hospital and Melbourne Health (1989- ) and Austin Health (2015).
Tertiary education
1967 B.Med.Sci.(Physiology) (First Class Honours), University of Western Australia.
1970 M.B., B.S., University of Western Australia.
1977 M.D., University of Western Australia.
Honors and awards
Masters has won many prestigious prizes and awards, including the Potamkin Prize of the American Academy of Neurology (1990), the Max Planck Award of the von Humboldt Foundation (1991), the Zülch prize of the Max Planck Society (1995), the Faisal International Prize (1997), the Alzheimer Award from the University of Munich (1998), the Lennox K Black Prize from Thomas Jefferson University (2006), the Grand Hamdan International Award (2006), and the Victoria Prize from the Minister for Innovation, State Government of Victoria and the Smorgon Foundation. In 2008 he was awarded the Honorary Degree of Doctor of Letters from the University of Western Australia. He is active in the Australian Academy of Science (AAS) and the Australian Academy of Technological Sciences and Engineering (AATSE), and continues to lecture widely at undergraduate and postgraduate levels. He has been appointed by the Australian Government as Chair of the National Health Committee, principal committee of the National Health and Medical Research Council of Australia.
Topic: The Molecular Origins of Alzheimer’s Disease: When Does It Start and What Strategies for Primary Prevention?
Abstract The etiology of Alzheimer’s disease (AD) is best understood through the deposition of Aβ-amyloid (Aβ). There are two basic forms of AD. The common (>95%) form is sporadic, and is caused by the failure to clear Aβ (mean age at onset 80 years). The rare (< 5%) autosomal dominant familial form is caused by the over-production of Aβ42, also on a background of failure to clear (mean age at onset 45 years). In both forms, the kinetics of Aβ accumulation are similar, taking about 30 years to accumulate a total of approximately 7mg of Aβ. Thus we estimate that sporadic AD starts about the age of 50 years and the autosomal dominant form starts about 15 years of age. The advent of validated biomarkers (PET/CSF Aβ and tau) now provides us with unprecedented opportunities for preclinical diagnosis, enabling the development of primary and secondary prevention strategies. Predictive algorithms utilizing age, biomarkers, polygenic and vascular risk scores are now being developed from longitudinal cohort studies to estimate times of onset and rates of cognitive decline. Applications of biomarker screens (blood, CSF, PET) to subjects who are about to cross the lower cutpoint threshold will define a population who may be suitable for primary prevention clinical trials.
Therapeutic targeting the Aβ pathway remains the principal strategy for delaying onset of AD. There are many molecular targets in this pathway, and no single one is likely to prove efficacious on its own. Therefore, a combination of strategies needs to be developed and applied.
Therapeutic targeting the Aβ pathway remains the principal strategy for delaying onset of AD. There are many molecular targets in this pathway, and no single one is likely to prove efficacious on its own. Therefore, a combination of strategies needs to be developed and applied.
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