Tuesday, 9 September 2014

MS Day What's new in the Lab

This year UCL our UCLP partner hosted the 5th Barts Research Day.They chose the venue, the format and the speakers

In contrast to what had been done previously the Research Day 2014, was in my opinion not really so much about research.

The topics had a feel that were more general, although with a healthy smattering of our clinical research.

The Lab based science was split into two themes QMUL research and UCL lab-based research.


Its a difficult one to balance giving new data that is light years from the clinic.

Professor David Baker 


Q&A:
A lot or most of the people that on MS drugs already, if you add in another drug, do you have to look at the safety right from the start again because you have a combination now of 2 drugs, for example?

We don’t have to go all the way round the board again. When you are doing testing you may do it on top of the drugs, so you will get that safety information. Because drugs do interact with each other, it is a part of development process to make sure that the drugs are safe. If you think about it, as in many other diseases, at the early stages it’s like a straight disease modifying drug and maybe few symptomatics, but as time goes by the drugs will be layered on top of each other, I think.

Do you have any thoughts on statins and blood lipid levels, bad vs good cholesterol?


The question with statins is knowing exactly how the drug works. We did some work with statins ourselves and thought that maybe the action has nothing to do with cholesterol synthesis; it’s just that one of the precursors that creates cholesterol was involved in the process of getting cells into the brain, and if you interfere with that process, cells cannot get into the brain. I think with the progressive trial there is another mechanism as well. If you look for example at Alzheimer’s disease genetics, there is a link perhaps with cholesterol synthesis, immune function and few other things. I think we have to learn a lot more about what statins are and what are they doing. ‘I do not know’ is the answer.

If a lot of your research is trying to get through the fat layer, brain barrier, why can’t you then go straight into the brain?

It is a bit drastic. Baclofen is a good example, you pump it into the spinal cord, but it’s a very expensive procedure and we cannot just keep injecting into the spine. The point that I am trying to get across is that we can use these properties in order to make drugs have a better side effect profile. By just getting the drugs in and then seeing how they work, and once we see they do work, we can try to make them better.

What is the chance of the whole drug development thing being quicker than 10-15 years, in the future? Is there any hope for that, because it’s quite a long time?


How would I speed it up? I would get the regulators to make it less of a tedious process. For example, why do we need to have 3 trials for some drugs? If we can make do with one trial for progressive MS for example, this will make it quicker and cheaper. This is one way, and then in terms of how we do the first bit? Well obviously we need to use science to speed this process up, and it can be done. Some of the companies, once they have an idea, they push these things along really quickly, as they can do them at the same time. When we did it we had to do one step, then wait to get some money, go to the next step and wait again to get some more money. With pharmaceutical companies, time is very important, so they do all of the steps simultaneously. It also depends on what the target is. So for our symptomatic drug we have planned our trial to get done within a month, when it is for neuroprotective drugs we don’t really know how long trials need to be, maybe a year or if we are to do a proper trial it can be 3-4 years, we don’t know.

What is your blog address?

www.ms-res.org

Presentation 2 Professor Kenneth Smith, UCL


Results too top secret to talk about?



More Videos to Come

19 comments:

  1. Mouse,

    I wonder if these research days have had their day. I note that Imperial and Cambridge are also holding research days this month. I imagine that funders require some engagement with patients. However, a familiar patter is emerging. There is always a speaker who talks about the licensed therapies and their efficacy / safety + therapies which will be licensed soon (and their efficacy / safety) + commentary about risk / benefits.... Then then there is the presenter who runs through the issue of how long it takes to get an idea to a licensed drug (20 years / £xx hundred million)...


    Most of the above is known to those who follow research. What do patients really want to hear about? I'm guessing they want to hear about things which might improve their lives i.e. When will drugs to halt progression be available? Is repair feasible and if so when will therapies be a available? Will I ever be able to ditch my wheelchair? Many of the presentations at the UCL event were rehashes of presentations I'd heard 5 years ago. As the world of MS research is so slow, I'd suggest research days take place every 3 years. At least there should be something new to report. I predict that if annual events continue, the attendances will drop off. MSers want to hear about things which will improve their lives - a run through of licensed drugs or the reasons why getting a drug to market is so slow has been done to death. When I see some attendees in wheelchairs and a presenter states that it will take 15 years to get a new spasticity drug to trial, I cringe.

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    1. I suspect the reason why Imperial and Cambridge are having research days is as a direct result of our teams commitment to public engagement with MSers that we have been doing for a number of years now. That there are more of these events can in my opinion only be a good thing. We know the pace of change is slow and could be better but I think an important part of these events is for MSers to meet others and to share tips on how they manage their MS. There are also usually breakout tables where more specific questions can be put on a one to one basis.
      On another note, the fact that some (see above) do not wish to make their presentations generally available is totally against the spirit of the event.

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    2. Anon I agree with you in part and your responses have been noted....However next year we will have results of two trials directly fromour research ....and if you have to cringe...I'm sorry but if you feed off the media "cure of the week" then you expect a result next week...I am sorry but this is not the reality...If I could change this I would

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  2. I agree with poster above that these conferences all seem to look very similar. What breakthroughts are coming? What might be here in 5 or 10 years time? You are the experts. I don't need a run through of current dmts or the usual excuses why things take so long.

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    1. Comments noted - we are planning something very different for next year!

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  3. Where is the video for Professor Kenneth Smith's presentation

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    1. Some presenters did not want to be filmed....sorry.

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    2. He lists demyelination, inflammation & degeneration as causes of symptoms.

      It's the first time I've come across this idea of different causes and it seems very important.

      But the slides on their own are not enough to understand it and the different types of recovery

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  4. A question to prof. MouseDoctor - it is difficult to get through the blood-brain barrier but Gadolinium MRI contrast manages brilliantly and targets active MS lesions selectively. How does it do it? Is it the quality of Gadolinium ( metal) or the proteins it is packed with?

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    1. Gadolinium gets in where the blood brain barrier is leaking and that is what it is designed to do. In health it does not get in so you see no lesions. How can you do this gaolinium is just a dye and as plasma (water) gets in the brain so does the dye. However normally water movement into the brain is limited because the blood vessels have a fatty coat and this repels water

      This is a good analogy. Now image our drug is like gadolinium and when the barrier is leaking it gets in. We have designed it so it only goes where the blood brain barrier is leaky however unlike gadolinium which is essentially measuring fluid movement and as you get swelling in the CNS gadolinium gets in, our drug will also get into lesions during progressive MS, because we have been more ingenious in how we do the targeting.

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    2. Intriguing, I like the sound of this. What is the drug/molecule or can't you tell us yet? When are you hoping to publish research about this?

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    3. Published this year. Here's a link. Not open access sorry.
      http://www.ncbi.nlm.nih.gov/pubmed/24287115

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  5. If your drug can selectively go into the T2 lesions as well, that's really cool :-)

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  6. The data is published (Al-Izki et al 2014 Brain) and that is why we could talk about it, , but before getting carried away. This is a prototype drug and it is not good enough in terms of its pharmacokinetic properties to be taken forward. It needs chemical tinkering but shows a new principal that could be applied to oother drug targets.

    Can this be developed...the problem is the perceived failure of the lamotrigine trial (How could it of worked if only 40-50% of people were taking the drug). If phenytoin or PROXIMUS comes off then interest will resurface.

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    1. If the drug needs enhancing lesions to get into the brain then will it be much use as a neuroprotective?

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    2. As the blood-brain barrier seems to be compromised even in inactive lesions, then there's a likelihood it will also get into the CNS in these areas too. It needs more work!

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  7. The slides talk of flashes of light when your eyes are shut as an MS symptom.
    Is this something different from the patterns you see on closing your eyes?
    I thought that happens to everyone

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    1. If it is a symptom, I wish somebody would have told me, I keep ending up at the hospital eye clinic with a suspected retinal detachment!

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