This year UCL our UCLP partner hosted the 5th Barts Research Day.They chose the venue, the format and the speakers
Professor David Miller:
Why the drugs do not have any benefits for Primary Progressive MS?
You are quite right. Some of these drugs have been tested in Progressive MS, i.e. Betaseron, Copaxone, and we needed those trials. There is a trial on Fingolimod which is about to finish a 3 year trial - and the results will be known later this year. There is also a Natalizumab trial in secondary progressive MS which is on the way and the results will be known in another year or so. So it hasn’t be proven yet that these more potent treatments are not effective in progressive MS, they might yet be, we have to wait for these trials. The reason that you cannot rely on the effective treatments for relapsing MS in progressive MS is that it seems to have a fundamentally different mechanism. In relapsing MS, the process closely relates to immune-system lymphocytes causing targeted damage in the brain but it seems in progressive MS this is no longer primary mechanism. There is rather more diffuse inflammation within the brain itself, which involves different cells, resident cells called microglia, which become inflamed and this causes an ongoing damage to the nerve cells. It is something different and we need to understand it more. I shouldn’t say too much as there will be more talks about it as the day goes by.
Why the white blood cells are attacking our brains? Why does it happen?
It is a very good question actually. I have no idea really. I suppose you could put it in another way - what is the cause of MS? The point of the damage seems that the immune cells are coming and doing that. The question is of course, what makes them do that. Autoimmune diseases are common in our society, they maybe more common than they were years ago, it’s a phenomenon of the modern world, the way our bodies interact with the changing environment, and of course the immune system, which is normally very disciplined and organised and only fights foreign material, foreign antigens, for some reason gets a bit upset and starts attacking our own tissues, like it might be diabetes in pancreas, rheumatoid arthritis in joints, psoriasis in the skin and in MS it is the myelin. There seems to be some susceptibly factors for that, such as certain genetic factors, about 100-150 genes are linked to MS, they are weak associations but they are nearly all linked with control of the immune system. There are also some environmental triggers, which probably again are modulating the immune system, such as viral infections and low Vitamin D levels. There is however a still big gap in our knowledge – what causes MS!
Why would we change from Tysabri to Fingolimod? What are the treatments and chances of having PML and surviving it?
In general this comes up when people who are JC positive and who have been on Tysabri for more than 2 years and then it’s deciding, and it’s a very individual decision, whether to live with the risk and it is still only one in 150-200. PML is a very serious condition if it occurs as there is no treatment for it. It has a 20% mortality. In my experience some people will want to stay on Tysabri because their MS has just changed for the better completely and I understand and support that but then sometimes people feel really concerned too and there is this option to switch. We are still in the phase of getting experience of actually the safety and risk of switching but it does seem – there are quite a lot of new reports coming out – that if it is done within about a 2 month gap in between stopping one and starting the other, it seems for most people to work pretty well.
Labels: MS Research Day