Do we need to promote Myelin repair or will a good anti-inflammatory do the trick

Piraino PS, Yednock TA, Messersmith EK, Pleiss MA, Freedman SB, Hammond RR, Karlik SJ. Spontaneous remyelination following prolonged inhibition of alpha4 integrin in chronic EAE.J Neuroimmunol. 2005;167(1-2):53-63.

Inhibition of alpha(4)beta(1) integrin blocks immune cell influx into the CNS providing benefit to patients with multiple sclerosis and in animal model systems. We have used this mechanism to examine whether the presence of inflammatory cells suppresses spontaneous myelin repair in experimental autoimmune encephalomyelitis. We observed (1) 87% of plaques showed remyelination after 40 days of treatment; (2) myelin repair occurred in half of the total lesion area; (3) half of the animals regained motor function. There was no significant repair or gain of motor function in vehicle-treated animals. Therefore, prolonged inhibition of CNS inflammation, in the absence of targeted myelin repair, facilitates mechanisms of spontaneous remyelination

You keep telling TeamG to get off its bum and start reporting on repair strategies. However this study suggests that one of the most important strategies to promote repair is to stop further damage occurring and then let the natural repair mechanisms kick in. 

This was shown using tysabri is EAE. The big question is does this happen in MS? 

The answer should be to hands. Some pathologists could have the answer, but have they looked? 

Tysabri can be very effective at stopping MRI lesions and relapses,which should allow repair to occur if this is the case. 

Unfortunately Tysabri also kills some MSers because of PML. Therefore how many demyelinated MS lesions are there compared to how many lesions that are remyelinated. This can determine if effective tysabri allows remyelination, or is demyelination persistent?

There clearly are some demyelinated lesions in PMLers based on one study but have pathologists really looked for remyelination. 

This is an experiment that needs doing urgently!

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  • Prof M,

    I was one of the posters who made a comment that Prof G needed to shift his focus to repair. I think that the guys in Cambridge have developed a highly effective treatment for those with RRMS – it just needs to get NICE approval and then prescribed by neuros. While I admire Prof G's determination to promote early highly effective treatments, I also want to see treatments come out of Team G i.e. not just involved in trials of agents identified elsewhere. Repair is the big empty space which needs to be filled.

    I've come across another website – MSnewschannel – overseen by a neuro called Timothy Vollmer in Colorado. I really like his approach:

    "In the past it's been years of therapy to simply slow the rate of progression of disability and the number of attacks. We have now in our center adopted a strategy that our goal with the patient is actually to stop the disease and put him into what we call a disease-free state. That means they're not having attacks, they're not accumulating new disabilities and their MRI's are not changing. That's not possible in everybody, but it's possible probably in at least two-thirds of patients and this is the
    first time in history that's been the issue."

    This guy and his clinic are implementing hit early and hard. The biggest scandal in the UK is the timidity of MS neuros still stuck in the "start with interferon" approach. Those of us in the UK look with envy at the approach (and results) adopted by Dr Vollmer clinic. We wonder why UK neuros don't put the interests of their patients first, or, at least, give them the choice. Perhaps Prof G should practise what he preaches i.e. start giving patients this option. Change will only come once the great and the good see the benefits. I know the answer will be that "the regulators / funders won't allow it". As a patient this is of no interest to me, patients should be given the best chance of keeping well. Be brave Prof G. The worse they can do is take away your practising certifcate – not a problem as "they" don't allow you to practise anyway – you are told what to do by a committee which does not have the interests of patients at heart.

    • Treatments like cannabinoids, beta interferon you mean?

      Guys in Oxford (Herman Waldman) actually developed CAMPATH whilst in Cambridge and the neuros did not invent the treatment or come up with the idea.

    • Unfortunately, it is acknowledged that interferons are modestly effective at best.

      Treatments based on cannabinoids aren't available to people with MS.

      Charcot Project may be Team G's big breakthrough.

      I just think anti-inflammatories are yesterday's news. Treatments to stop / slow progression and treatments to encourage repair are the next step toward the holy grail of putting this disease to bed.

      Hopefully, we'll see some breakthroughs soon. I just want Team G to be in the forefront of the new area of treatments.

    • Treatments based on cannabinoids aren't available….sativex is a cannabinoid me thinks

      Cladribine worked as well as any DMT and had side effects like any DMT it was licenced but it was the company that withdrew it.

      We have a number of investigator led trials ongoing on progression, planning another today you can't do everything

    • Mouse,

      As you're a nice guy and Christmas is coming, I won't annoy you further. Fingers crossed your spasticity drug comes good and you become a rich man.

    • Yes fingers crossed….I can't say how it is going until phase I is finished… to being rich I'm not holding my breath

      Happy xmas to you too I'll send a card

  • As someone who is on Tysabri, isn't the easiest way to find out for the neurologist to monitor the EDSS score for users on a regular basis. Perhaps we could all update our chart on-line for comparison, as it is our own interest to find out the answer.If we thought we were getting better the power of the mind might take us on another level.

  • Once axons have been demyelinated, they may be forever changed including when they are remyelinated:

    The change seems to be a redisribution of sodium channels which results in an increase in the energy consumption of the axon. Over time this higher demand of energy kills the exposed axon.

    To me it seems like the priorties are as follows:

    1. Prevent damage to the myelin as early as possible.
    2. Find a way to reduce the damage caused by the extra energy required by exposed axons so they don't burn out.
    3. Remylination of demyelinated axons.

  • Progress with anti inflammatories is wonderful, but you have a cohort of ppms and spms people who are also looking for answers that help them.

    • Which are at the forefront of all our research efforts in this lab. progress is being made but of course it can't be soon enough.

By MouseDoctor



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