This blog is part of our Symposium Blogathon series – where we are counting down to the 33rd International Symposium. Numbers in bold blue type correspond to the code in the abstract book. Click on the number to be redirected to the full abstract.
Every year, one of the highlights of the Symposium is our plenary speakers. This year we have 15 ALS/MND research and clinical care experts who will be presenting their research.
To give you a teaser of what is to come, we will be taking a closer look at each of our plenary speakers over the next two research blogs. In each blog we will explore the topics they will be presenting and find out a little bit more about the speakers.
Day 1, Session 1: Opening Session
The 33rd International Symposium on ALS/MND kicks off on the Tuesday 6 December and begins with the Stephen Hawking Memorial Lecture. The Stephen Hawking Memorial Lecture aims to bring experts from outside the immediate world of ALS/MND research, to help stimulate new ideas and research collaborations. Over the past few years, the Memorial Lecture has included speaker such as 2020 Chemistry Nobel Prize Winner, Dr Jennifer Doudna and Dr Rudolph Tanzi, Harvard Professor and world leader in the genetics of neurological disease.
This year the Stephen Hawking Memorial Lecture will be given by Dr Fred Gage, President of the Salk Institute. Dr Gage and his team investigates how the adult central nervous systems is adaptable to different environmental stimulation throughout its life. His work uses cutting edge stem cell techniques to model human diseases in the brain and central nervous system to help further our understanding.
In his talk ‘The contribution of aging to neurodegenerative disease’ (C1), Dr Gage will describe the development of models of neurones that are representative of neurones found in people with Alzheimer’s disease. Models of disease are so important in understanding the biology of neurodegenerative disease, such as ALS/MND and Alzheimer’s disease, as it is not practical take samples of neurones from living donors. Being able to create accurate models of the diseases allows researchers to further our understanding of what happens to the neurones during the disease.
Day 2, Session 3: Metabolism
There is an increasing amount of research that suggests people living with ALS/MND have hypermetabolism. This is where the body is burning energy at a higher rate than it normally would. Some research has also suggested that this disruption to metabolism can also be linked to a poorer prognosis (more rapid illness).
In her talk ‘Dysregulated energy metabolism related to worse prognosis in ALS’ (C6) Associate Professor Shyuan Ngo, from the University of Queensland, will discuss the impact of energy metabolism on prognosis in people living with ALS/MND in more detail. She will also touch on how understanding more about energy metabolism in people living with ALS/MND has the potential to be used in a clinical setting as a tool for prognosis.
Day 2, Session 4: Cell Based Models
Dr Kasper Roet is the CEO and co-founder of QurAlis Corporation. He is also co-founder and serves on the board of directors of EnClear Therapies. Dr Roet has specialised in gene therapies and stem cell technology-based precision medicine solutions for neurodegenerative diseases.
In his talk ‘iPSC-derived models for compound screening’ (C9), Dr Roet will discuss the use of induced pluripotent stem cells (iPSCs) neuronal models. iPSCs are skin cells that have been reprogrammed in a dish in the laboratory into motor neurones. Dr Roet uses these motor neurones to test and identify potential new treatments for ALS/MND. Earlier in this blog we mentioned how using models of ALS/MND can help us understand more about the disease, in this talk Dr Roet will highlight how models can be used, alongside new technologies such as machine learning and artificial intelligence, to discover new drugs. It is hoped that using these types of models and technology will lead to effective treatments.
Day 2, Session 5: Disease Presentation and Risk
To end the second day of the Symposium, we have a session on Disease Presentation and Risk with all 3 of our speakers presenting plenary talks.
The first to present is Professor George Davey Smith, from the University of Bristol. In his talk ‘Identifying risk factors using Mendelian randomisation’ (C12). He will discuss how mendelian randomisation approaches can be used to understand disease onset and disease progression. Mendelian randomisation is an approach which uses variation within genes to assess whether a particular factor (such as high cholesterol) could be a cause of disease. In this talk, Professor Davey Smith will review current approaches and discuss how mendelian randomisation could be useful in investigating and prioritising therapeutic targets for ALS/MND based on causes.
Next up is Dr Carmela Tartaglia, from the University of Toronto. Recent research has suggested potential links between contact sports, such as rugby and football, and ALS/MND. This has led to some discussion on the impact of head injury and concussions on ALS/MND, as well as other neurodegenerative diseases. In Dr Tartaglia’s talk titled ‘Traumatic Brain Injury as a Risk Factor for Neurodegenerative Disease’ (C13) she will present an overview of the research into traumatic brain injury and will highlight what research is needed in this area. Particular attention will be given to chronic traumatic encepthalopathy (CTE), a slowly progressing neurodegenerative disease which occurs after multiple concussions, and how understanding CTE could help in understanding the relationship between concussions and other neurodegenerative conditions.
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The final plenary speaker in this session is Dr Michael Benatar, from the University of Miami. Currently, diagnosing a person with ALS/MND is difficult, as there is not a simple diagnostic test and often people are only diagnosed after often experiencing physical symptoms for several months. Emerging research indicates that ALS/MND begins with a pre-symptomatic phase, where the person does not have physical symptoms of ALS/MND but the disease is active within them. It is only sometime later, once a significant level of neurological damage (neuron loss) has occurred that we see physical symptoms (the clinical symptomatic phase). In Dr Benatar’s talk ‘Mild Motor Impairment and Prodromal Disease Markers’ (C14) he will describe how mild motor impairment, which includes minor motor abnormalities that are initially not severe enough to be classed as ALS/MND, could be a useful diagnostic tool before a full diagnosis of ALS/MND.
Day 3, Session 6: Genetics and Genomics
In order to find effective treatments for ALS/MND, it is essential to understand the biological pathways that are going wrong in the body. Within our bodies, there are networks which work to control gene expression (control when genes are active or switched off), which ultimately manages the function of the cell. When things go wrong in ALS/MND, gene expression can be changed which results in cells behaving differently to how they should, which can lead to motor neurones dying.
Dr Janine Kirby, from the University of Sheffield, will be presenting a talk titled ‘Decoding gene regulatory networks in ALS’ (C15). Dr Kirby will discuss how using a technique called gene expression profiling could be used in clinical trials to understand the mechanism of action of the treatment being tested and explain variations between patient responses. She will use the example of the IMODALS clinical trial to highlight how the different responses in the clinical trial were linked to changes in gene expression in the patients.
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