Unrelated Blogger Comments October

Sometimes you want to say something unrelated to the Posts then this is the spot for you.

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  • I noticed that some of the warnings for Alemtuzumab show that "you must tell the doctor if you have diabetes" does this mean that those who have multiple sclerosis along with diabetes will not have access to this drug, or does it just mean different monitoring protocols/doses? I wanted to see if I might be excluded based on having diabetes along with relapse remitting multiple sclerosis.

    • Prof. G Just seen you sitting in the business class lounge waiting for your flight. I assume business class to Copenhagen care of one of the Pharma Companies?

    • Unfortunately, economy class care of MS in the 21st Century; a lobby group to improve MSer or patient engagement. I am feeling very tired, which is why I haven't posted anything yet today.I only got home last night from our Basildon Roadshow at 22h30 last night and was up at 4.30am this morning.

    • Profg travels so much he has access to business lounge whether flying business or coach.
      This comes from years of business travel.
      Look out for me in the toilets.

    • Re diabetes. Not aware of diabetes being a contraindication to alemtuzumab. However, it would have to be controlled diabetes.

  • Related to Brain atrophy.. This PR from TEVA today might be of interest

    " "These analyses reinforce our faith in the potential of laquinimod and we are proud to announce that we plan to initiate a clinical trial of the drug in PPMS to gather even more evidence of this novel mechanism of action," said Dr. Michael Hayden, President of Global R&D and Chief Scientific Officer for Teva Pharmaceutical Industries Ltd. " We also believe the potential neuroprotective benefits of laquinimod could have significant application in the treatment of other diseases like Crohn's disease, lupus nephritis, Huntington's disease and Alzheimer's." "


  • The information in Why Grey Matter Matters (My first infographic) tells a lot of stories How many of us know all those facts and figures together with the consequences


    • Mouse Doc went to Geranium as a guest of ECTRIMS and I went to Noma as a self-funding citizen. I turned down the ECTRIMS faculty meal at Geranium to experience Noma.

    • I did not get any Pharma Dinner or Drinks……although I got loads of coffees a couple of fruit smoothies and swiped a few free pens from the Pharma stands.

      Having just had time to read my emails, I realise I missed an opportunity,.

      I would like to thank ECTRIMS for their invite to participate in the meeting.

  • Charcot Project: INSPIRE Trial – Raltegravir / Isentress

    I am about to commence Month Three of taking Raltegravir and whilst I have no idea what my MRI scans are showing, I KNOW I feel far more myself than I’ve felt in the 2 years I’ve had RRMS and I KNOW that my performance has improved in both the cognitive and physical tests carried out as part of the trial. Aside some legacy issues with my arms and hands (symptoms that have been with me since January – the drug isn’t supposed to fix existing myelin damage), the rest of me feels NORMAL again. Most significantly, my head feels clearer and I feel free of that dragging fatigue that has plagued me since I first felt symptoms.

    I am back working full hours full time at the office, after working reduced hours for several months. Friends and family have remarked how “I am back!”, because I once again have the energy to be me. I surprised myself by subconsciously planning a hiking and camping trip for next spring – activities I enjoyed pre-MS, but things I haven’t had a single thought about doing since MS struck.

    I was wary about feeling “good” during the first few weeks of the trial, because even though the trial doesn’t include a placebo group, I was aware that “the placebo effect” might be an issue, i.e. I am taking a drug, therefore I must feel better. However, I am confident that how I am feeling is real.

    If anyone is umming and ahhing about whether to volunteer for the trial, I would advocate going for it. We are all different, so have different symptoms and stages of this disease, so I will only speak for myself, but my rationale for volunteering was very simple: I want to be symptom free for the rest of my life. I don’t want to be “OK” for 15 years or so and then rapidly succumb to SPMS: I want this bl**dy disease to go away! I can’t expect neurologists, researchers and the much-derided pharma industry to magic a cure without helping out by being a guinea pig, so I’ve decided to take an educated risk. I hope some others of you will join me!

    If any of you don’t know what I’m talking about, here’s a link:

    • Thanks for posting, good to hear 'from the horse's mouth'! Thanks also for participating so that this research can proceed – I only wish I could but don't fit the criteria.

      Please post again in a few month's time.There are many of us keeping an eye on this research.

  • Professor G, what role does EEG test play in MS? Along with blood flow tests?
    The Italian Journal of Neurological Sciences
    1998, Volume 19, Issue 6 Supplement, pp S413-S417
    EEG correlates of cognitive impairment in MS

  • I've been listening to the short reports on various topics from Ectrims shown at MS World forums. These are targeted at patients. I've received useful information. I have to say, I prefer the tone and content of the material I find here. You don't talk down as much. I understand that there is a broad target audience, but many of us are well educated professionals. Even without much education, most of us are adults, quite capable of comprehending our prognosis and using what information we can find to try to mitigate it.

    This leads to a question. How does reluctance by doctors to share bad news factor in to the neurologist – ms patient dynamic? With my own diagnosis, by a general neurologist, it seemed he did not want to believe I had MS, possibly because he didn't want me to be ill. Since then, he's been more than helpful in facilitating many kinds of treatment, but much less forthcoming with his assessment of how I'm doing.

    It's worked out well enough, but without this blog and other resources, I would have known much less about what sort of help might be possible and so what symptoms to highlight and questions to ask. I don't distrust his good intentions or willingness to help, but I do question his honesty with regard to hard facts. If he's trying for placebo effect, it may be counterproductive as I really don't trust what he says about how well I'm dong at this point.

    Any thoughts would be appreciated.

  • Lemtrada will cost $95k in Germany?

    "Sanofi has confirmed that its new multiple sclerosis treatment Lemtrada (alemtuzumab) will cost approximately $95,000 for a full course of treatment in Germany, where the product has now launched. Cost per vial of Lemtrada is $11,700, with patients typically treated with eight vials over a two-year period."


    I doubt it will be first choice for MS…

    • It looks a high price, but since my first in fusion in 2006, I've gone 7 years without a relapse and EDSS stable (no disease activity on MRI). I still work full time. I was on Rebif for a year c.$ 12,000 and kept on relapsing. Lemtrada appears to give long term remission for some.

    • Remember there is also a strict monitoring process every month for 5 years so this will also add to the cost.

      This interesting as it was "How much?" Was a question they did not want to be asked.

      You also have to put this in context as was 7 years on from 2013 at 12 x 7 = $84,000 and interferons dont cost $12,000 any more

  • Lemtrada ??? – sibling diagnosed with ITP at age 7, in the days when there was no treatment and we almost lost her, upon her entering adulthood serious on going herpes simplex such that whole face and scalp infected, remitting at the moment, and the trifecta, I was diagnosed with MS. Siblings with immunological perfect storm. So no Lemtrada for me, not really wanting to add ITP to the grab bag – am I right to be fearful?

  • Thank you Prof G. I was aware that ITP could be a stand alone – however it was her additional herpes simplex, plus the MS that I have which had me looking for dots to join. I thought I would report it as you have an interest in the herpes family diseases. Ausimmune wanted to get extension funding to include siblings but alas couldn't raise the amount required.

  • Prof g and Prof mouse,

    I'm sure all the followers of this blog would be grateful for a quick summary of what came out of ECTRIMS 2013. Is there any feel that those of us with MS can any more hopeful – ie we are getting nearer to really understanding the disease / getting nearer to treatments which make us a bit better. Sad to say that I'm also becoming a little sceptical about these conferences. Looks like a good time was had be all the attendees, but little of real value to those of us with MS. Leaves a bad taste in the mouth when the researchers who still cannot identify the cause of the disease / the cure are living it up in top notch restaurants while those with the disease are living on benefits. Guessing they remove conscience when at neurology school.

    • These conferences are not for the benefit of MSers but are there for the benefit of neurologists to meet and learn. Many of them may not be research active. Neurologists and other clinicians need to continue their education.

      As to excesses there are clearly many and this is a big difference between a clinical meeting and a basic science meeting. Many researchers do not go to these meetings and more often than not the restaurants of the masses may be a fish and chip/Pizza shop or a sandwich.

      The degree of creature comforts are vastly different. I am not sure I get to see hospitality areas which are clearly present at ECTRIMS etc.However this is a meeting of prescribers, which is the business of pharma.

      The abstracts on which there were thousands are on the ECTRIMS website and will filter through but it depends if you want science fiction or science fact.There will be a will be a host new DMT

  • Prof G,

    You believe that Laquinimod may be neuroprotective and is potential blockbuster. However, when i read the study results c.35 per cent reduction in brain atrophy it doesn't seem that impressive i.e 90 per cent reduction would impress me. Would a higher dose achieve better results? Am i misunderstanding the drugs effectiveness?

    • From how I understand it, this drug could be a blockbuster because it could be used as an additional therapy to current drugs. So, hopefully it can reduce atrophy 35% on top of the benefit from the other DMT used. It would be able to be prescribed to all MSers, not just the % who decide to use it as their primary DMT, like with the other drugs.

  • " [0157] In this study, each compound alone shows a dose dependent inhibition of disease severity. However, while the lower dosages tested (0.06 mg/kg laquinimod and 25 m/kg DMF) are moderately effective individually; the combination of DMF and laquinimod when each is administered at the respective lower dosage is so potent that it completely abrogated disease. This unexpected result suggests that lower dosages of laquinimod and DMF can be used in combination to achieve a greater than additive therapeutic result, and provides evidence that such a combination can be used for therapeutic treatment of human MS and CIS patients. "


    Very promissing data! Another combo patent application with Gilenya shows simular data. Can it be possible for TEVA to make a LAQ/DMF combo oral? Or will TEVA have to agree with Biogen Idec before making such product?

    Since DMF is not a new substance in Europe ( Fumaderm ) I guess it is possible that TEVA will be able to market a combination of DMF and LAQ in Europe. Maybe the best possible DMT ?

  • Profs,

    I would be interested in one of your think pieces on remyelination therapies. I've heard about the Biogen anti-lingo trial, my friend who is a patient of Dr C has been asked to participate in a gsk remelination trial. Today there is news about a Parkinson's drug which may promote remyelination. Not sure if Prof Franlin's work focuses on remyelination. With so much going on (early stages) any observations welcome.

    • Fingers crossed that some will work.
      The Anti-lingo is a front runner but does enough get into the CNS to cause remyelination. It has and pharma behind it as does the GSK being co-ordinate d by Sir Jeremy.

      I suspect the studies will not be in addition to anti-inflammatory treatments and so my be asking a lot we shall see.

    • It's a presentation of MRI research using five levels of analysis instead of one as McMasters did. By separating the MS groups into nonstenotic and stenotic, they're finding a significant difference between the stenotic MS group and the healthy controls.

      Benztropine is search term not found perhaps more comments on this as its in the news enough I asked Neurologist about it.

      a drug called benztropine, which is already available as an approved treatment for Parkinson’s disease. Once the researchers homed in on benztropine, they confirmed that the oligodendrocytes it had coaxed into maturity could in fact make myelin when in a dish with neurons. The team then analyzed benztropine’s activity in a mouse model of MS, finding that it diminished the clinical severity of the acute and remission phases of the disease while pretty much eliminating the relapse phase. In this model system, benztropine worked at least as well as the immunosuppressive drugs now in use to treat MS

    • Here was a post on this on Tuesday, 15 October 2013. I was away when it came out the week befre



      "Disease while pretty much eliminating the relapse phase. In this model system, benztropine worked at least as well as the immunosuppressive drugs now in use to treat MS"

      Yes I agreed but they claimed it was not immunosuppressive when it looks like an immunosuppressive. This was also the case for the orignal stem cell papers. There were claims about repair but if you looked at the data to me the data showed immunosuppression. 5 years later and it was reported in loads of places that the stem cells were working by immunosuppression.

      In this study they report that there is no effect on immunosuppression and there is inflammation in the CNS but no clinical disease this is very unusual…I have seen it once with a drug that inhibited clinical but this was not reflected by such an inhibition infiltration and even then there was not such a great clinical effect.

      As they mention the drug can have side effects. Were these so high that they stressed the animal such that its EAE stopped. I believe this happens a lot in the EAE literature.
      You can show it works on the recceptor becaaus that is what makes the animals unwell and stressed. I do not know if this happens in this case. Lets say not until proven otherwise

      The human dose is 1-5mg/day so that is about 0.1mg/kg- 0.01mg/kg and they used 10mg/kg so that is between 100 to 1000 times more than a human gets. Even allowing for a ten times difference from more to man this is a big dose and makes you concerned about the translatability and so do not start self-medicating as this is of unproven value andthe drugs will have side effects as they interfer with nerve signalling

      You can see the graphs so in figure 1.If they dose when dose was givenduring the time of disease induction it essentially wiped disease away, but when given after one of the control group when most of animals were probably healthy it did not stop them getting sick but animls did not relapse which would be immune driven. If the drug was just working by remyelination why the disconnect? If disease hasn't started in both cases there woulld be no demyelination and remyelination would therefore start at the same time in both cases but there is a big difference in the clinical profile…why?. As an immunosuppressive this data would be consistent with the literature that the therapeutic canbe too late for the first phase but can stp the second phase.

      As a word of caution the pictures are supposed to be representative of whats going on but they do not necessarilty mean anything as even in a sick mouse I could find an area with no infiltration and another area with infiltration.You cherry pick thepictures to show what you want to say. Hwever they have done quantitation so lets accept what was done.

      If you look at the myelin ratios they come pare treated to untreated during theattack and it looks different by treated animal looks just like the remission animal with no treatment is time the healer.

      So lets see this repeated. I bet if we did RXR-related drugs we could get a similar effect but in this case there is evidence thathighdoses are immunosuppressive.

      However the other data supports a potential to aid myelination

  • Is Sativex still licensed for MS and could it be prescribed for nerve pain ? Generally speaking

    Regards as always

  • Professors,

    Do you know if there is any 6 month EDSS data published on BG-12 ( Tecfidera )?
    I can only find 3 month EDSS data and find it quite strange because 6 month data is available for Aubagio, Tysabri and Gilenya.


  • Dame Sally Davies, the government's chief medical officer, is advocating free Vitamins (esp Vit D) for all UK children under 5 years old. This is aimed mainly at tackling the increase in rickets. Will it help MS? Is the dose high enougg? Can we use this government intervention to prove that Vit D has a role in MS? (or, in 20 years time, if there is less MS because of better Vit D, will the debate still rage on because nobody made this into an experiment?)

  • http://www.news.wisc.edu/22163

    a team of UW-Madison biochemists has discovered a promising vitamin D-based treatment that can halt — and even reverse — the course of the disease in a mouse model of MS. The treatment involves giving mice that exhibit MS symptoms a single dose of calcitriol, the active hormone form of vitamin D, followed by ongoing vitamin D supplements through the diet. The protocol is described in a scientific article that was published online in August in the Journal of Neuroimmunology.
    Hayes' team tried a weekly dose of calcitriol. They found that a weekly dose reversed the disease and sustained remission indefinitely

    So what do you think Professor G and Mouse Dr? Is Professor H team onto something thats worth $150 of calcitriol to be injected once for chance to be free of MS?

  • I will have a look next week but when i hear reverse and eae together be warned it is generally over hype. I can do the same with a salt solution.
    Lets see

  • Do you know if there is any 6 month EDSS data published on BG-12 ( Tecfidera )?
    I can only find 3 month EDSS data and find it quite strange because 6 month data is available for Aubagio, Tysabri and Gilenya.

    • To the best of my knowledge the 6-month EDSS progression data has not been published or presented. I will ask Biogen-Idec for the data. However, this was not a pre-planned outcome measure.

    • Gallet al Noninvasive transorbital alternating current stimulation improves subjective visual functioning and vision-related quality of life in optic neuropathy

  • I was looking for brain atrophy data for different DMT's/candidates and wonder if there is data (placebo controlled, not post-hoc ) for Aubagio, Tysabri and Tecfidera? I can only find data for Gilenya and Laquinimod.

    Can you help me out?

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