The 24th International Symposium on ALS/MND was the most successful to date with over 950 clinicians, healthcare professionals and scientists attending the meeting in Milan.
There was a ‘hive’ of activity on social media this year with over twenty researchers ‘tweeting’ during the event and fourteen of them reporting on our peer-to-peer blog ReCCoB. We also contributed by tweeting updates throughout the conference using the hashtag #alssymp. You can view the tweets from the symposium here (even if you don’t have a Twitter account!).
With over 100 presentations and nearly 400 posters there was a wealth of clinical and scientific research discussed during the symposium. Networking amongst researchers also stretched out over coffee and lunch breaks, with a number of new international collaborations formed by the end of the meeting. Read More »
If you followed the reporting about the symposium last weekend, I’m willing to bet (but I haven’t checked!) that most it will have been about the talks that people attended or liked. When actually, a large proportion of the research presented at the International Symposium on ALS/MND is in the form of a poster.
A poster is a hard copy of a research study, it can be the latest results or developing a new methodology. It’s quite often a PhD student’s introduction into presenting their work face to face to their peers.
Following the day’s talks, on the first and second evening of the symposium, it was time for an opportunity for some informal networking around the posters. At allocated time slots presenters stand by their work and explain it to fellow delegates. (They also have time to visit other posters too).
For twenty of those presenting posters, there was an additional pressure. They were on the shortlist for the International Symposium Clinical and Scientific Poster Prizes respectively.
With Pantomime season kicking off back home in the UK, delegates in Milan were introduced to one of the newest cellular villains in the MND story – oligodendrocytes.
Although oligodendrocytes were first identified in the 1920s and are known to be affected in multiple sclerosis, they were generally considered as ‘bit part’ players in MND rather than ‘centre stage’.
All that has started to change in the past couple of years, with researchers in the USA and Belgium independently showing that, in both SOD1 mice and human post mortem MND brain tissue, the brain was making new oligodendrocytes to replace ones that appeared to be dying off. The problem is that the new ones being formed appear to get stuck in an immature state and therefore do not perform their role of helping motor neurons to maintain appropriate energy levels and also send electrical signals down their long nerve fibres.
So, by getting stuck in a ‘Peter Pan’ scenario of never growing up, oligodendrocytes may be at best, unable to help protect the death of motor neurons or, at worst, they may actually contribute to the degeneration. Peter Pan rather than Captain Hook as the pantomime villain is a novel twist to the script!
The results of new research investigating a link between physical activity and MND was presented by the University of Sheffield research group in the late-breaking news session on the last day of the 24th International Symposium on ALS/MND. Under the leadership of Prof Pam Shaw, along with Dr Chris McDermott, MND Association-funded researcher Dr Ceryl Harwood presented her findings.
The background of MND and physical activity
Physical activity and the link between MND has long been debated amongst researchers.
There are a number of different types of physical activity; from leisure time (for example an evening walk) to more vigorous physical activity and athleticism (marathon runners and professional sportsmen).
Previous research back in 2008 found that Italians playing professional football had an increased risk of developing MND. However, this research is yet to be confirmed in other countries. Director of Research, Dr Brian Dickie said: “The Italian researchers also looked at professional cyclists and basketball players, but no association was found, so basically the jury has been out on whether athleticism is a risk factor for MND.”
The International Symposium on ALS/MND is a showcase for the international MND research and clinical practice community to get together and present their latest findings. Questions after the talks often spill over to the coffee breaks, lunch, the bar at the end of the day and breakfast the next morning.
Add to this there are many separate events going on, taking advantage of the fact that they know that this is one place that everyone is likely to be there. For example on Thursday afternoon there was an afternoon meeting of the European Network to Cure ALS (ENCALS), and different meeting later in the evening. Even today, the last day of the conference, at least three official breakfast meetings were going on at 7am.
In light of all of these opportunities to network, organising a mini-networker for delegates was almost creating a Russian doll of networking – you come to the Symposium to network, then, within that there’s another opportunity to network, then within that etc – I hope you get the idea. It was nothing grand, a glass of wine or a beer and a few sofas.
Plenary speaker Dr Massimo Filippi put this question to delegates on the second day of the 24th International Symposium on ALS/MND.
Opening the session on neuroimaging, Dr Filippi gave an excellent review on what we currently know about this area of research, and ultimately answering whether or not we can see more clearly in MND?
It’s all in your head – Magnetic Resonance Imaging (MRI)
Over the past ten years there have been significant advances in the identification of neuroimaging patterns in MND. Dr Filippi focused mainly on the use of MRI neuroimaging (a technique used to visualise changes in the brain). He stated: “Through the use of MRI we have been able to detect cortical thickness of the Cerebral cortex (the outermost layer of the brain), which is significantly reduced in MND”.
We know that in the 5-10% of cases where there is a strong family history of MND, there is likely to be a genetic cause at work, acting like a weight to push the scales in favour of the disease occurring. These gene mutations are hidden somewhere within the 15 billion or so letters of DNA that make up our genome and, through collecting samples from extended families affected by the disease, coupled with huge advances in gene-hunting technology, researchers have managed to identify over two-thirds of the causes of hereditary MND in recent years and are hot on the heels of the other causes.
When you hear the word ‘cluster’ the first thing that comes to mind is probably a group of stars – not MND. During a plenary talk by Dr Ettore Beghi on Saturday 7 December the question was: ‘Is there anything we can learn from clusters in MND?’
What do we mean by clusters?
Dr Beghi began his talk by defining a cluster as “a health related event with temporal or geographical activity.” Meaning: a number of people are diagnosed with a disease in either a specific time period or area. He also highlighted that if rare diseases are found in clusters then this may require environmental factors to be investigated.
We already know that MND is thought to be caused by a combination of subtle genetics, environmental and lifestyle factors. At the MND Association we regularly receive enquiries about apparent ‘clusters of MND’ and I was looking forward to hearing Dr Beghi’s talk on the subject.
A packed room at the 24th International Symposium on ALS/MND was given a fascinating whistle stop tour covering stem cells, robots and cellular garbage clearing, by Dr Steve Finkbeiner of the University of California, as well as a glimpse into the future of developing ‘disease in a dish’ models of MND.
Dr Finkbeiner outlined how his lab is attempting to conduct “clinical trials in a dish” by generating huge numbers of cultured neurons cells for automated ‘high throughput analysis’ of their health and death. As he says, “we’re basically trying to develop a comprehensive physical examination for nerve cells”. Read More »
A characteristic sign of motor neurones affected by motor neurone disease is the clumps of protein visible down a microscope. Although these proteins have been observed in motor neurones from people affected by MND since the earliest descriptions in the 1870s, a key discovery was made when the identity of a protein, common to all types of MND, was unveiled as ‘TDP43’ in 2008.
Two years later a second protein called FUS was also been found to be common to all types of MND. More information on this aspect of MND can be found in an article on our research blog.
One of the exciting things about these two discoveries was that they were both linked to a set of biological pathways, known as RNA processing. The was the first major clue that RNA processing was involved in MND. When the discovery of genetic defect in the C9orf72 gene came along in 2011, that made a third MND-causing gene defect that linked to RNA processing.
The first session of the 24th International Symposium on ALS/MND after lunch yesterday was dedicated to the topic of RNA processing and dysregulation. Several of the talks presented work on understanding the role of TDP43 in MND.