Sunday, 1 October 2017

Unrelated Comments & Questions - October 2017

Sometimes you want to say something unrelated to the thread or ask a clinical question or some other MS-related question that has not been answered in past. This is the place for you.


75 comments:

  1. Can Alemtuzumab cause gaot? Given the debris caused by the dead lymphocytes circulating in the blood. Surely this is one side effect that's not been documented? I am 3 weeks post treatment and wondered my symptoms are coincidental or Due to treatment?

    ReplyDelete
    Replies
    1. Oops meant gout. Damn predictive text! As opposed to bad at spelling?

      Delete
    2. Yes, it can. Gout is due to crystals of raised uric acid forming in the joints. When alemtuzumab lyses cells the DNA that is released has to broken down and this leads to increased uric acid levels. In general this is really only a problem when alemtuzumab is used to treat lymphomas with a high cell or tumour burden. In MS the cell burden is much lower and gout is uncommon. However, some pwMS who are predisposed to develop gout may develop gout after alemtuzumab and other cell depleters. Please note this is only likely to happen in the first few days after being treated with alemtuzumab; at 3 weeks this is likely to be due to another cause. I have seen joint pains and arthralgias in several patients post alemtuzumab. It is usually self-limiting and clears spontaneously.

      Delete
    3. Hmmm strange. My first and only gout attack was 9 years. I decided with a heavy heart to stop beer. Instead took up wine. Been alcohol free for 4 weeks. On Alemtuzumab diet free of meat. Eat a lot peanuts though. Some reason get a yearning for them. On the plus side isn't high uric acid indication of no ms activity! If so will take it even if the foot pain is unbearable!

      Delete
    4. Is TB something else that should be flagged up with Alemtuzumab.
      Saw MS nurse Friday who mentioned they've had four patients test positive for TB between 1st and 2nd round of infusions. Consequently I was tested for it Friday, alongside everything else.

      Delete
  2. Is it possible/common for onset of cognitive fatigue/issues to occur as long as a decade before other clinical signs of MS? Mental activities got more draining/hard over the years, where now I can't even read a book without it being taxing. But 10 years before just seems so implausible and I'm hesitant to bring it up with my neuro as to not come across as crazy

    ReplyDelete
    Replies
    1. Yes, cognitive fatigue can be part of the MS prodrome that can last years.

      Delete
  3. MS newbie here! What is considered "inadequate response to the treatment" given that NEDA is not achievable over long term? Consequently, how is the decision to switch from one DMD to another made?

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    Replies
    1. Who said NEDA is not achievable over the longterm. With high efficacy therapies, rebaselining and treat-2-target the majority of patients can be rendered NEDA-2 or NEDA-3. The question is still open regarding NEDA-4, -4, etc.

      Please note that a lot of NEDA studies are in the injectable DMT era and an era without rebaselining or treat-2-target.

      Delete
    2. Please use the blog search function with the following search terms to read up on NEDA.

      NEDA #ClinicSpeak

      Delete
    3. @MS newbie, 1230 PM:

      http://jamanetwork.com/data/Journals/NEUR/932709/noi140092t3.png

      Delete
  4. Does Ocrelizumab really cause Breast Cancer? How big of a risk is there? Where can more information be found on this? Is it something I should be worried about? (Typing breast cancer and ocrelizumab is proving to be unhelpful as I don't know who to believe) I'm told by my neurologist that I may be able to start once it's available on the NHS but hearing about the cancer risk is putting me off. I know there was a post on rituximab on the blog but I couldn't find anything on Ocrelizumab itself.

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  5. I don't know. But we have covered this issue on the blog before.

    http://multiple-sclerosis-research.blogspot.com/2017/07/researchspeak-b-cells-and-breast-cancer.html

    ReplyDelete
  6. Was reading the Wikipedia page for DMF, and found it states "Phase III clinical trials found that DMF (BG-12) successfully reduced relapse rate and increased time to progression of disability in multiple sclerosis (trade name Tecfidera).[5][6]" (https://en.wikipedia.org/wiki/Dimethyl_fumarate)

    As I know you are interested in MS nomenclature and untruths on the internet,
    I thought Id mention it, particularly as the reference is your paper.

    ReplyDelete
  7. At Team Barts, what do you currently offer to any of your progressive patients as treatment plan in terms of Dr. G's treatment pyramid?

    How do you follow these patients along over time to know if your treatment plan is effective as course of progression in individual patients is so variable. IE. MRIs of grey matter/atrophy, clinically (9 PEG, EDSS, 25 foot walk test) and NFLs on LP?

    ReplyDelete
    Replies
    1. In terms of of progression and the pyramid there is nothing licenced for progressive MS (in EU) that can go on the bottom. In our PROXIMUS trial it is any DMT

      Delete
  8. http://multiple-sclerosis-research.blogspot.com/2017/08/clinicspeak-dietspeak-could-diet-be.html#comment-form

    2017/08

    "There is emerging evidence of that intermittent ketosis and fasting may have general health benefits, which include potential benefits for pwMS. I, therefore, plan to do a series of posts on diet and nutrition in relation to MS over the next few months"

    This month? Next maybe?

    Obrigado
    Luis

    ReplyDelete
  9. I am currently taking Copaxone but recent MRI has shown disease activity. Having read your posts on Cladribine, I am very keen to take this as the off-label injectable and I'm prepared to pay for it if necessary. Would I have to be referred by my own GP to your team at Barts and travel to London to access this treatment if my own consultant says it is not available where I live? Do you think the oral equivalent will be available in 2018 or later? Thank you for your time and best wishes to all at Barts.

    ReplyDelete
    Replies
    1. DrK may be able to answer your question.

      Apparently the oral version can already be a private prescription in UK according to the people from Merck.I don't know the cost.

      As for the NHS there will be the haggle with NICE it's label is only for highly active...

      Delete
    2. Drug should be available privately, there was an advert in Practical Neurology for the UK market. Current price tag is £2,047.24 per 10mg tablet; pack of 4 costs £8,188.97; pack of 6 costs £12,283.46. As the dose is weight adjusted (https://www.medicines.org.uk/emc/medicine/34044) the cost for a 70-80kg person would be £28,661.36/year; double that (£57,322.82) for the complete course (28 tablets). I don't know whether the NHS will pay that much, or get a (usually undisclosed) discount.

      Delete
    3. Alemtuzumab type use. alemtuzumab type price. I guess.

      Delete
    4. Anon 7.28
      If you're RRMS ask your neuro if you qualify for escalating treatment? Eg to fingolimod or dmf?Off-label cladribine inj sounds great doesn't it? If you are RRMS and qualify for something else your neuro would have to justify use of off-label (assuming willing to prescribe it).

      Crikey, look at the cost of those tablets! Crazy money.

      Delete
    5. So the cheaper off-label subcutaneous Cladribine would not really be an option for me/not currently accessible at all in the UK? Would 'highly active' MS be classed as having a heavy lesion load on MRI and having failed more than two DMT's?

      Delete
    6. Anon 5.56
      Go to the web version of the blog, click on the tab about cladribine. There's a Barts MS NHS document that explains about off-label cladribine injections. Print it out and take to your neuro for discussion if you're interested.

      Re highly active MS, there are criteria to meet. Try searching the blog or MS Trust website.

      Re off-label cladribine inj accessible in UK, no real reason why it shouldn't be but in practice places don't seem keen. Might be different when Ravenclad licensed for those 'lucky' enough to qualify for it, why shouldn't those who don't qualify not have equally effective off-label injections?

      Delete
  10. It would be great if you could do a future post on treatment options after an MSer has received their two initial cycles of alemtuzumab in an induction approach to treating to relapsing MS. How do you decide whether to initiate a maintenance drug versus waiting for evidence of disease activity before initiating a third cycle of treatment? Do you have any preferences with respect to the different maintenance drugs that should be initiated after the first two cycles of treatment with alemtuzumab? Can you anticipate that ocrelizumab might be an appropriate or safe maintenance drug to use after alemtuzumab? Could ocrelizumab help avert the onset of secondary auto-immunities that can emerge after alemtuzumab?

    ReplyDelete
    Replies
    1. ProfG may respond as it is something he has been thinking about.

      I think the situation is that we can only prescribe the two infusions as NHS England won't pay for any more. This is daft as we know that about 50percent of people will need a third dose. The data from Cambridge seem to indicate that three doses will sort out about 85percent of people so it is crazy that people don't get third dose. If you go maintainence afterwards what is best.

      We proposed a number of things to try and reduce the autoimmunities a
      .One proposal was to use rituximab. There was no interest in doing this at the time it was proposed. Maybe things are different now.

      Delete
  11. T cells transfer dopamine to B cells to produce antibodies

    https://www.nature.com/nature/journal/v547/n7663/full/nature23013.html

    ReplyDelete
  12. Transcranial direct current stimulation reduces fatigue associated with multiple sclerosis (?)

    https://medicalxpress.com/news/2017-10-transcranial-current-fatigue-multiple-sclerosis.html

    ReplyDelete
  13. I thought gout and ms were mutually exclusive?

    ReplyDelete
  14. The role of T follicular regulatory cells at how autoimmune disease develops

    IL-2 promotes FoxP3+ regulatory T (Treg) cell responses, but inhibits the differentiation of T follicular helper (Tfh) cells. However, it is not clear how IL-2 affects T follicular regulatory (Tfr) cells, a cell type with properties of both Treg and Tfh cells. Here we show that IL-2 prevents, rather than promotes, the development of Tfr cells. Using an influenza infection model, we found that Tfr cells were barely detectable at the peak of the infection, but accumulated as the immune response resolved. High levels of IL-2 at the peak of the infection promoted the expression of Blimp-1 in Treg cells, which suppressed Bcl6 expression and thereby precluded Tfr cell development. However, as IL-2 levels declined some CD25+ Treg cells down-regulated CD25, up-regulated Bcl6 and differentiated into Tfr cells, which prevented the accumulation of self-reactive antibody-secreting cells. Thus, unlike its effects on conventional Treg cells, IL-2 inhibits Tfr cell responses.

    http://www.jimmunol.org/content/198/1_Supplement/152.8

    https://medicalxpress.com/news/2017-10-autoimmune-disease-viral-infection.html

    ReplyDelete
    Replies
    1. This simplified...

      "The team discovered that about a week after the infection, levels of an immune regulator called the IL-2 protein increased. This triggered the multiplication of common regulatory T-cells, or Tregs. When this phase of the immune reaction was fading, TFR cells started multiplying, reaching peak numbers about a month after infection.
      The formation of the TFR cells was therefore tightly linked to the processes controlling Treg production, researchers said, with falling levels of IL-2 allowing the new phase of the immune response.

      The TFR cells migrated to the lymph nodes — the headquarters of antibody-producing B-cells. Here, B-cells proliferate and change their antibody-producing genes to create new, stronger antibodies. But sometimes the gene changes, or mutations, give rise to an antibody that attacks the body, instead of invaders.

      Researchers discovered that TFR cells prevented B-cells, which gave rise to autoantibodies, from accumulating in the lymph nodes. Importantly, the TFR cells had no impact on the immune processes targeting the influenza virus.

      When researchers prevented TFR cells from forming or removed them from mice, the animals started producing autoantibodies, they explained."

      Delete
  15. This seems important

    By scanning the brains of healthy volunteers, researchers at the National Institutes of Health saw the first, long-sought evidence that our brains may drain some waste out through lymphatic vessels, the body’s sewer system. The results further suggest the vessels could act as a pipeline between the brain and the immune system.
    Dr. Reich’s team plans to investigate whether the lymphatic system works differently in patients who have multiple sclerosis or other neuroinflammatory disorders.

    “For years we knew how fluid entered the brain. Now we may finally see that, like other organs in the body, brain fluid can drain out through the lymphatic system,” said Dr. Reich.

    https://www.technologynetworks.com/neuroscience/news/the-brains-meninges-harbour-its-lymphatic-system

    ReplyDelete
  16. Lymphatic network to the brain is nothing new. Common knowledge I thought?

    ReplyDelete
  17. Does BMI, gender and following the OMS diet affect Gilenya. I have many days sick and thought maybe it could become too effective because of BMI of 19 and the other above mentioned factors?

    ReplyDelete
  18. Why is ocrelizumab taking so long to be approved by EMA? Their more than 6 months behind FDA. Surely they must have sla? Not to mention patient lives to consider.

    ReplyDelete
    Replies
    1. There are clearly issues and that issue must be PPMS,do they buy the activity?.

      Delete
  19. Fast Forward, a non-profit subsidiary of the National Multiple Sclerosis Society, will give financial support to TG Therapeutics to advance TGR-1202 (umbralisib) into preclinical testing as a potential oral therapy for progressive forms of multiple sclerosis.

    TGR-1202 (umbralisib) is an orally available PI3K delta inhibitor, targeting the delta isoform with nanomolar potency and several fold selectivity over the alpha, beta, and gamma isoforms of PI3K. The delta isoform of PI3K is strongly expressed in cells of hematopoietic origin and is believed to be important in the proliferation and survival of B-cell lymphocytes. Inhibition of PI3K delta signaling with TGR-1202 has demonstrated robust activity in numerous pre-clinical models and primary cells from patients with hematologic malignancies.

    Umbralisib has been successfully combined with TG-1101 (ublituximab), an engineered antibody that targets a specific sequence on the CD20 protein found on immune B-cells, on cancer.


    http://www.tgtherapeutics.com/publications.cfm

    ReplyDelete
    Replies
    1. Fastforward are ace and saved us when we were about down and out.
      However if it is preclinical it is years away for being an ms drug.

      Delete
    2. Yes, and the money they donated are far from being enough to support a trial. If the company has no interest in running it, it can take a long time. TG-1101 is close to be released but I dont know what extra can offer with Ocrevus and -soon- Arzerra around.
      It is interesting as a combination therapy though and I am wondering if FF chose it for progressive forms to fill the drug gap or there is some extra benefit on progression to it.

      Delete
  20. Evolutionary medicine

    Endogenous retroviruses and their role to human evolution and diseases

    https://www.nytimes.com/2017/10/04/science/ancient-viruses-dna-genome.html

    ReplyDelete
  21. Innate immunity in overdrive?Saturday, October 07, 2017 7:57:00 pm

    I am diagnosed with PPMS. As a child, I regularly developed severe wheezing with viral infections. But as an adult, I never develop full blown colds or coughs. I can't remember the last time I had a cold requiring a box of tissues. At most, I am just tired and briefly have a mild sore throat (usually in the early hours of the morning, before I get up). What does this say about my immune system?

    ReplyDelete
  22. I have been reading today that "Almost half (45%) of people with MS feel they have experienced mistreatment or stigma because of their symptoms, according to our most recent survey. " (MS Society 2016).

    I have MS and experienced discrimination recently about my MS. This was from someone who should know better.

    ReplyDelete
    Replies
    1. What surprises me about this survey is that the figure is so low!

      Delete
  23. Do you know more about the patients who had breast cancer in the ocrevus trial. I recently found out that one of them had tested positive for brca gene. Do we know much about the others?

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    Replies
    1. Had thought their ages would have been all over 50 which is a risk factor but no some were early 40's. Other risk factor is breast tissue density..they really should have screened for these risk factors.

      Delete
    2. @adambomb - What is your source for this? Can you please post it? Can teamG verify the statement above?

      Delete
  24. Clemastine fumarate as a remyelinating therapy for multiple sclerosis (ReBUILD): a randomised, controlled, double-blind, crossover trial(?)


    The primary efficacy endpoint was met with clemastine fumarate treatment, which reduced the latency delay by 1·7 ms/eye (95% CI 0·5–2·9; p=0·0048) when analysing the trial as a crossover.

    http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32346-2/fulltext

    ReplyDelete
  25. Has anyone heard of this study, sounds interesting, and low risk
    https://overcomingms.org/first-drug-shown-promote-remyelination/

    ReplyDelete
    Replies
    1. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32346-2/fulltext?elsca1=tlxpr

      Delete
  26. There are quite a few posts on this blog about clemastine - type clemastine in the "Search this blog" box next the top of the page on the left - and then ponder why this promising treatment hasn't been further investigated (and I'm not having a go at Team G here, so please don't misinterpret me about that)

    ReplyDelete
    Replies
    1. Simple reason...we do not work on remyelination at present and therefore it is not on our radar.

      It is a old drug and so there is no pharma interest in old drugs...they take the surprising approach of using antibodies that are 99.9% excluded from the CNS:-(

      However, the study poses questions and surely this deserves more study to get answers. A lovely piece of basic science leading to useful clinical outcomes

      Delete
    2. We don't work on remyelination...should we have a go and see what it does to chronic EAE. Does this mean we should start prescribing this? Pharam wont be interested, unless they get can make money out of this, so let's see what happens. Why haven't we reported on this...Ari Green has been asked to do a guest post, however profG has been slacking with a response,as I am sure you are all asking why can''t we have this drug now.

      Delete
    3. Clemastine is an over the counter drug. (this is not spam MD et al!)

      Delete
    4. Exactly, anonymous, there is no profit in this for the pharma companies. So should we be asking more of our MS Societies, to fund research into drugs that pharma will never consider? Would this work? (That is a genuine question, by the way, I would appreciate your thoughts, everyone)

      Delete
    5. You have had MS Societies funding CCSVI, sem cells, statins why not?

      However how good are the results, are they clinically meaningful?

      Delete
    6. So how do we get clinically meaningful results? (Again, genuine question) - all these promising old drugs just seem to go nowhere after the first brief flurry of interest - it's very frustrating for pwPPMS, the answer could be out there, but no-one looks....

      Delete
  27. p://www.express.co.uk/news/science/712930/head-transplant-scientist-Frankenstein

    Charlatan or Pioneer?

    ReplyDelete
    Replies
    1. The Italian face of stuff done in China. Mice rats and now dogs. Not of the faint hearted...just as well they don't live in UK they would need protection from the anti-vivisections and quite a few others.

      "Dr Canavero managed to reconnect the severely damaged spinal cords using a chemical called polyethylene glycol, or PEG"

      PEG is commonly known as anti-freeze.

      It is is used as a glue when making antibodies and as a carrier of interferon beta.

      https://www.ncbi.nlm.nih.gov/pubmed/28612398
      Polyethylene glycol-induced motor recovery after total spinal transection in rats. Ren S, Liu ZH, Wu Q, Fu K, Wu J, Hou LT, Li M, Zhao X, Miao Q, Zhao YL, Wang SY, Xue Y, Xue Z, Guo YS, Canavero S, Ren XP.CNS Neurosci Ther. 2017 Aug;23(8):680-685

      I note the lead authors are all from China

      Immunohistochemical evidence of axonal regrowth across polyethylene glycol-fused cervical cords in mice. Kim CY, Oh H, Ren X, Canavero S.
      Neural Regen Res. 2017;12(1):149-150

      Delete
  28. http://www.foxnews.com/health/2017/10/16/why-americans-with-ms-are-going-to-russia-for-treatment.html
    stumbled across this on the internet. "Broadly speaking there are two types of MS: RRMS and progressive MS"
    Bruce Bebo, the head of research for the NMSS of the U.S. still stratifies MS into relapsing and progressive MS. The one thing that needs to happen is for MS to be considered one disease as Prof G has been harping on. Hopefully ECTRIMS 2017 will unify neuros on this point. Lastly, you can read between the lines that HSCT is facing serious head-winds from pharma and insurance companies.

    ReplyDelete
  29. http://m.jpost.com/HEALTH-SCIENCE/Israeli-developed-ALS-treatment-reversing-motor-decline-breakthrough-507678

    The beginning of the end of MS as neurodegenerative disease?

    ReplyDelete
    Replies
    1. It is company stuff so I am not going to comment or post on this, but it is stem cells that have been engineered to make growth factors, the phase iii trial has started this month, so lets hope it is positive

      Delete
    2. "The beginning of the end of MS as neurodegenerative disease?"

      Maybe for mice..people???

      “These stromal stem cells are more flexible, and that’s why, although they represent less than 0.1% of those cells in the bone marrow, we take them, we expand and purify them, we produce tens of millions of those, and then we try to inject them. First we tried in the mice models of multiple sclerosis and it was fantastic.”..“We saw that paralyzed mice regained their walking and jumping abilities, so this means that these cells induce recovery and prevent damage to the nerves.”

      Not sure about this but there's a ppms patient claiming to
      have restored 7 years of progression with the stem cells.

      "Now in his late 40s, the dual Israeli-British passport holder and a former marathon runner had sought help from many sources to fight MS, but had been told in Britain that “they had nothing at all to offer” other than a little help from speech and physical therapists or cholesterol tablets."

      https://www.jpost.com/Jerusalem-Report/Opening-a-door-to-regenerative-medicine-459639





















      Delete
  30. Women are dangerous to men.....Beware.....

    https://jamanetwork.com/learning/video-player/14836123?utm_source=silverchair_information_systems&utm_medium=email&utm_campaign=new_issue&utm_term=featured&utm_content=sidebar

    Obrigado

    ReplyDelete
  31. Programmed death 1 is highly expressed on CD8+ CD57+ T cells in patients with stable multiple sclerosis and inhibits their cytotoxic response to Epstein–Barr virus

    Growing evidence points to a deregulated response to Epstein–Barr virus (EBV) in the central nervous system of patients with multiple sclerosis (MS) as a possible cause of disease. We have investigated the response of a subpopulation of effector CD8+ T cells to EBV in 36 healthy donors and in 35 patients with MS in active and inactive disease. We have measured the expression of markers of degranulation, the release of cytokines, cytotoxicity and the regulation of effector functions by inhibitory receptors, such as programmed death 1 (PD-1) and human inhibitor receptor immunoglobulin-like transcript 2 (ILT2). We demonstrate that polyfunctional cytotoxic CD8+ CD57+ T cells are able to kill EBV-infected cells in healthy donors. In contrast, an anergic exhaustion-like phenotype of CD8+ CD57+ T cells with high expression of PD-1 was observed in inactive patients with MS compared with active patients with MS or healthy donors. Detection of CD8+ CD57+ T cells in meningeal inflammatory infiltrates from post-mortem MS tissue confirmed the association of this cell phenotype with the disease pathological process. The overall results suggest that ineffective immune control of EBV in patietns with MS during remission may be one factor preceding and enabling the reactivation of the virus in the central nervous system and may cause exacerbation of the disease.

    http://onlinelibrary.wiley.com/doi/10.1111/imm.12808/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER

    ReplyDelete
  32. Many MS patients suffer from migraines


    Migraines may be the brain's way of dealing with oxidative stress

    https://medicalxpress.com/news/2017-10-migraines-brain-oxidative-stress.html

    ReplyDelete
  33. MIS416, another drug that aimed to decrease the action of T cells via the TLR-9 and NOD-2 pathway failed Phase 2B

    http://www.proactiveinvestors.com.au/companies/news/185913/innate-s-multiple-sclerosis-trials-prove-unsuccessful-new-direction-sought-185913.html

    ReplyDelete
    Replies
    1. Thanks for the info

      There is "one direction".to go but it's not the British Popgroup.:-)

      Delete
  34. A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis

    Highlights

    •HDAC1 has a novel pathophysiological role in EAE.
    •Mice with a T cell-specific deletion of HDAC1 are completely resistant to EAE.
    •Selective inhibition of HDAC1 might be a promising strategy for the treatment of multiple sclerosis.

    Eighteen HDACs take part in the epigenetic process of turning genes on or off. In addition to regulating gene activity, they can change the activity and function of proteins. The bottom line is that they play a major role in regulating a cell’s behavior.

    http://www.sciencedirect.com/science/article/pii/S0896841117305954?via%3Dihub

    ReplyDelete
    Replies
    1. Thanks for this but I generally do not post on EAE cures of the week because their are too many and because even if they are amazing it is light years away from MS.

      Importantly I come across as a grumpy old geezer (person) when all around is saying amazing.

      Get rid of T cell function and you get rid of EAE, but if MS is not T cell driven then is it relevent.

      Delete
  35. Just watched the Taubman Prize lecture by Dr. Hauser. Wonderful journey on how B-cells came to be the driving force in MS and development of Ocrevus.

    Would be great to post on the Blog. I have no idea how to get the lecture. As Dr. G was mentioned in the credits, maybe you can reach out.

    Debbie

    ReplyDelete
    Replies
    1. I,ll have a look. Was it mentioned that anti CD20 was shown to be active in rheumatoid years before the studies in MS.

      Delete
    2. Yes. He was recognized for his 20 year achievement in pursuing where the science led him. It was very compelling and for many of us not in the thick of the research very informative. And so hard to think that for so long he/others were told it could not be B cell driven.

      Just wanted to share.

      Delete
    3. Thanks, we will see him at the burning debate, if you find a youtube link if it was filmed post the link.

      I hear he is writing a book, maybe that is why profG went to meditation.

      Delete

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