Interest in dementia research has come to prominence over the last decade and is now being coordinated through the National Health and Medical Research Council’s National Institute for Dementia Research (NNIDR).
No topic was off limits at its inaugural Australian Dementia Forum 2016.
Leading international researcher, Professor of Neuroscience and Director of Sydney Brain Bank, the University of NSW and Neuroscience Research Australia (NeuRA), Glenda Halliday, presented her keynote speech on the highly contentious issue ‘is dementia contagious’?
“All human neurodegenerative diseases are proteinopathies, meaning they have abnormal aggregations of proteins commonly found in the brain,” Professor Halliday said.
“A small group of proteinopathies have been shown to be caused by prions, a highly infectious material made of protein (protein infection), which can be transferred to a healthy organism often through the environment and can then self-propagate and transmit its conformation to that type of protein in the individual, causing widespread neurodegeneration and inevitably death.”
Professor Halliday said these prion diseases, such as Creutzfeldt-Jakob disease and Kuru, have been shown to cross the species barrier and can be spread by direct contact with infected tissue.
“It is speculated that other neurodegenerative proteinopathies could behave in a similar way, like Alzheimer’s disease, but the most convincing data is for multiple system atrophy (MSA),” Professor Halliday said.
“This disease has misfolded alpha-synuclein, a common protein found in neural tissue, which is also the main pathology in Parkinson’s disease (PD) and dementia with Lewy bodies (DLB).”
Professor Halliday said although these three diseases (MSA, PD and DLB) all feature abnormal alpha-synuclein, the aggregates manifest in different ways, and potentially have different mechanisms in how the protein aggregates are formed.
“It has been theorised that in MSA the abnormal alpha-synuclein is less stable and this type of protein has been shown to be transmitted when injected into transgenic mice,” she said.
Professor Halliday presented the pros and cons of these theories and the relevance they may have in the way we look at these diseases at the Forum in Brisbane from 1-3 May 2016 there was some debate among researchers from the floor.
Professor Halliday joined fellow key note speakers Professor John Hardy from the UCL Institute of Neurology in London who won the Breakthough Prize 2015, and Professor Pierluigi Nicotera Head of DZNE in Germany as well as a number of NHMRC-ARC Dementia Research Development Fellows at the conference.
Professor Halliday said the NNIDR symposium provide an excellent forum for researchers with common goals to meet and share their ideas.
“It’s a great opportunity for the dementia fellows to present their future aspirations and provide a basis for future collaborations,” she said.
Professor Halliday is currently focusing on identifying early versus later events in neurodegenerative disorders, both aspects suitable to try and either halt disease onset or stop progression once the disease has begun, and also to more reliably detect the underlying protein changes in patients.
“A major component of this research is the development of biomarkers (biological markers) which when compared with non-diseased brains can give a wealth of knowledge into what is going wrong in the diseased brain,” Professor Halliday said.
Professor Halliday has been looking at blood biomarkers, MRI and molecular changes in brain tissue over time and with the new dementia team project will be expanding her studies to include families of affected people with the support of funds from the NNIDR.
“This is an exciting area, which has grown hugely over the last decade and has real potential to help change the lives of not only those affected but the future generations of these patients,” she said.