Q&A August 2020

Q

For those reading on 1 August. Happy Yorkshire Day

Gods Own Country

You know the the drill if you have a question unrelated to the threads. This is the place for you

About the author

MouseDoctor

138 comments

  • Well a’ll gu to foot er ah stairs… I didn’t know you were a Yorkshire man, MD.. Happy Yorkshire Day back at thi, me owd cocker! 🤣

  • JOIN ACTRIMS/ECTRIMS round the corner. Anything exciting to look forward too in pandemic causing misery at biblical proportions across the world. Like we have cure ms it was staring as in face all the time. Or should we rename the acronyms ACTRIMS/ECTRIMS to Consortium for Trade related investment measures.

  • Vaccines trials with pwms
    Is there a strategy to test any future covid vaccine on people with ms and specifically people on particular dmts?
    Or will they just be wrapped up with all the ‘routine’ studies/trials etc
    is there a plan?

  • Hi,

    I have no idea if this is a relevant question for this thread.
    Sorry if it is not and or if it is already answered elsewhere.

    Does unconjugated bilirubin, in case of hyperbilirubinemia, get into the adult brain/CNS or not?
    And if it does is it considered neuroprotective or neurotoxic?

    Thank you,

    With kind regards,

  • Hi
    Do you think there is any potential future benefit of cord blood banking? I’m currently pregnant and have just started researching whether it’s worth paying a couple of grand to do this in case things might develop this way in the future. Would appreciate your thoughts
    Thanks 😊

    • A load have people did this as it could a future source of stem cells for their children…..the companies doing.this have probably long since folded and the cells have thawed and been thrown in the bin, but you can make stem cells from any cells now.

  • Hi Mouse Doctor.

    I read your last post about memory B cells. I am pretty new on the blog. Can you explain to me your theory on memory B cells ? If I understand well to your mind B cells are the key target to keep MS at bay because they are driving the immune attacks ? So for you T cells only obey to the messages send by memory B cells that are infected by EBV ?

    If I understand well how your theory fits with the Prof G ´s idea of smouldering ms ? And if your therory is true why ocrelizumab are not better at reducing BVL in comparision with Alem ? Do you think BVL data would be different if OPERA would have been made 2 years after diag like for Alem ?

    Thanks in advance.

  • Is there a general “feeling” (if such a thing be allowed in science), that MS is a retrovirus, and therefore -as perceived by this patient -a malign for ce , changing its shape like the T 1000 robot in Terminator 2 ?

  • 1. Why are so many MS research teams across the world focusing all their time on Covid 19 to the detriment of research into MS (the real MS)? I’ll take my chances with Covid 19, I have no chance with MS given it’s progressive from the outset (unless a therapy to tackle smouldering MS comes to market).

    2. Where is Prof G?

    • 1) There is a judgement in your question I don’t necessarily share, i.e. that research into Covid-19 must be to the detriment of “the real” MS research. However, there has been (and still is) an urgent need to establish whether pwMS are exposed to greater risk, particularly with DMT. The evidence so far suggests that most DMTs are relatively safe, so teams can refocus on their core activity, which is how to understand and best treat MS (in a Covid-19 era).
      2) On holiday.

      • Thanks Prof K. As a non-scientist / researcher, it just appears that thousands of MS / Covid 19 papers are being published (often relating to tiny numbers eg 2 Alemtuzumab patients with Covid 19) and many seem to be published to (i) increase the publication list of an academic or (ii) allow an academic to show their knowledge of the immune response to viruses. Maybe I’ll be proved wrong and they’ll be some interesting MS work presented At ECTRIMS / ACTRIMS. Good luck with your research and trials.

        • You are wrong here the fact that someone developed covid 19 one week after alemtuzumab is highly informative as this person has no t or B cells yet they recovered in a week. Therefore these case studies can be highly.informative as it shows that peripheral blood T and B cells are not needed for recovery

          • Thousands of papers…..(1) about (
            100 papers and a (ii) fraction are from scientists… Are you having a dig again….it’s endless.

          • So, what’s the hypothesis? Cells migrate from the thymus Asia bone to fight the disease? Or innate immunity is somehow able to provide protection?

  • Hello, could you tell me if lesions caused by migraines enhance with contrast or is it only ms lesions that enhance. Is there also a connection between migraine and ms. Thanks

  • Hi,
    Is there there a link between recurrent lung infections and multiple slerosis other than aspiration pneumonia? I mean is there any immunological link?
    Thank you,

  • A Tysabri and Covid question, please. How should an individual weigh up the risks and benefits of switching to 6-weekly dosing (for Covid risk-management purposes) or sticking with the tried-and-tested 4-weekly? What factors should he/she take into account? And how good is the evidence basis for these decisions at an individual level?

  • If energetic stress can induce degeneration is it possible that overheating increasing energy needs of neurons has the same effect in the long term?

    Why many clinical trials start/end late with respect to plans or are not updated after planned completion date?

    Thanks

  • Happy Yorkshire Day MD, from a Yorkshire lass!

    Is there any other data released yet re anti CD20 and COVID-19 (related to death, as I think we have established risk is higher)

    Thanks!

    • In the cohort we found there were 5 deaths in over 400 cases and most of those had covid risk factors such as age etc.

      • Thanks.

        If someone was to consider delaying their next infusion of ocrelizumab (due in sept, would like to get winter over with before second full dose) – would you say having a blood test to measure B cell levels would be helpful or not?

          • Because I am a healthcare worker and as I understood it, I am (slightly) at less risk of covid currently 5 months since my last infusion. If I went ahead with my next I would be at higher risk at work and potentially have to ‘shield’ after the steroids etc. So basically I would delay as currently ocrevus isn’t particularly compatible with my work and covid risk.

            Oh and also I thought I had read on here that delaying does not adversely affect my MS as the effects last longer than 6/12?
            Perhaps I have got that wrong.

  • Another Ocrevus related question here from a fellow Yorkshireman. There’s been a lot of posts lately about the real MS, smouldering MS etc and the effectiveness of alem and HSCT in relation to Ocrevus. In some cases, they are being considered a potential ‘cure’. Is it the case that Ocrevus as a ‘maintenance therapy’ does not have the same potential in addressing the real MS? Happen us Ocrevus folks were to shift on to that there alem in’t future, are we at a disadvantage from playing the B side first?

    • Smouldering MS as I understand it would not be touched by alemtuzumab or HSCT so ocrelizumab may not be different. The study needs to be done

      • If smouldering MS was not addessed by alemtuzumab or HSCT, how could they end up with no disease progression over 10 years for a substantial share of patients (I assume we believe most if not all have smouldering MS in some degree)?

        • Because they are highly active at stopping the peripheral immune response causing damage in the CNS and stopping smoldering MS

  • Exercising is mentioned on this blog as benifitial for people with progressive form of MS. Is there any information about the intensity of this exercises? Does your heartbeat need to be elevated for 30 minutes daily to be succesfilm? What’s best? Are there any advices or guidelines?

    • I was diagnosed ppMS 8 years ago at age 55 and have since endeavoured to maintain an exercise regime of 200 km/ week on a traditional road bike. This involves an average of 2 hours/day on uneven terrain 5 days/week. I try to ensure that I develop substantial perspiration and get out-of-breath several times on each ride. I no longer use a heart monitor unfortunately so am unable to give any definitive data.
      The medics who monitor and know my condition hold me up as an example of a pwMS who is slowing his progression.

      • Some ppms happen to have a very slow progression..am sure some like you exercise and some do not. So to attribute your slow progression to exercise is maybe a “feel good” story..just because your exercise feels good does not mean it affects your ppms.

  • When discussing the increased longterm cancer risk among MS patients treated with immunosuppressant drugs, ProfG recently made an interesting comparison with a treatment for rheumatoid arthritis that has been around since the 80´s with similar depletion effects however an insignificant increased rate of malignancies.
    Unfortunately, I can‘t find this post any longer. Could you please jog my memory as to which drug he was referring to? Thanks!

  • Do you have any sort of roadmap for how to transition away from rituximab?
    After several years and over 10 rounds of treatment

    We try to increase the gaps between cycles
    Between cycles, the MS seems to disappear
    But the re-dosing eventually becomes necessary

    The IgG levels fall lower with each cycle

    How to transition, and to what?
    Is cladribine an option?
    Or alemtuzumab or HSCT?

    The question has become more pressing because of the pandemic

    • Don’t worry it will be there next year….but it’s been Yorkshire Day for the past two weeks, Leeds promoted last week and Harrogate Town today….what next? Chelsea to get a thumping in the champions League… 🙂

  • The possibility/desirability of my coming off fingolimod (to cladribine) has been discussed but I forgot to ask about the ‘exit strategy’. I am very, very worried about the prospect of the washout effects on my MS (had a mild version when transitioning from copaxone so am guessing at massive impact with fingo). Is there anything that can mitigate the effects?

  • I’m m not an native English speaker so, not sure what you meant. But what I know for sure is that mostly of my relapses ocured after gastro intestinal disturbances or antibiotics use, so I could not wondering if is any known connection. Thank you .

  • Hello,
    My wife has ppms with typical leasons in brain and spinal cord plus typicial liquor bands.
    Additionally she has positive MOG-antibodies.

    Sadly the neurologist does not know, what that means.
    1)Although I dont expect an advice on a personal case. But maybe you can explain in general, what you know about mog-antibodies and ms.
    2) Secondly would you expect, that with ocrevus, the MOG-antibodies should also disappear, because of the b-cell-depletion?
    Thanks a lot.

    • Dont hold your breathe…in the news item they say they want an inhibitor of the enzyme, inhihibt the enzyme and you have all sorts of neural defects add to this the protein is expressed outside of the nerves such as the immune system you will have unwanted side effects and for the drug to work it has to get into the brain and then the right cell….This is not an easy thing to do, so it is another “cure of the week” that is probably a million miles away from human treatment

  • Hello Mouse Dr.

    I have been following relevant postings concerning various DMT’s (specifically Ocrevus) and “vaccine readiness” for covid 19. There is a lot going on with facts running about, all over the place. But in all honesty, these facts usually leave me confused and without certainty as to a “final answer”.
    Simply- can you tell me, if one is 170 lbs and 62 years old, and had their first two half infusions (300 mg) of ocrelizumab, followed 6 months later (mid-September 2019) with a last standard 600 mg infusion, how long would it take their immune system to “rebound” to “normal” (all other things being standard, normal, “middle of the road” average), so they were “vaccine ready”?
    On a related ethical note, I was watching (here in “Trump-land”), a network special on the unfolding of the Covid pandemic. One of the commercials was for Ocrevus! I couldn’t believe they paired it with this special, and failed to mention anything about vaccine concerns. Given the covid programming, one with MS would almost have to assume that the advertiser would have said something if there were a concern. I found it very unnerving and crass. Or maybe I’m making too much of it.
    In any event, I look forward to your estimate on vaccine readiness for the situation mentioned above.
    Thanks, Tom

  • I am late for the August Q&A but I was just too curious. I came across some papers on complement inhibitors… what is your position about complement inhibitors in MS? Small and large molecules… could they affective an effect on smouldering MS in your opinion?
    Thank you!!!

  • Finally, a accurate and reproducible EBV load test is available. Time to put your money where your mouths are with ms and ebv link and conclusively end this debate? Or more dithering and excuses? Until pharma sugar daddy comes along to make it happen.

    https://www.globenewswire.com/news-release/2020/08/05/2072978/0/en/Roche-announces-FDA-authorisation-for-the-first-Epstein-Barr-virus-quantitative-test-on-the-cobas-6800-8800-Systems-to-improve-care-for-transplant-patients.html

      • Has barts and other research units considered going on BBC’s Dragons Den and pitch proof of EBV link to MS will lead to cure of MS and potential billion dollar sales. The offer them a percentage of revenue? Or better still approach Capital investment funds? Pharma is not the only sugar daddy around.

    • There lots of drugs that show positive effect on ms including metamorphic, lipoic acid, vitamin d, clemastine, plant based proteins, cholesterol drug, asprin, single malt Wiskey, etc, etc. MS society is another pharma like company protecting its revenues and therefore throwing red herrings out to prevent the research into a cure. There at least 1 in 10 people on metmorfin, yet there is no evidence those with ms have a lower edss scores of less severe relapses. The only thing close to a cure is alemtuzumab and HSTC.

      • It appears the cure for conspiracy theorists is just as elusive as a cure for MS.
        Let’s not get too carried away peeps.

        • Wouldn’t life be boring without the conspiracy theorists. At least they were right about ufos. US confirms their military bases are being stalked by unidentified Aerial phenomenon. Their words not mine. Truth is stranger than fiction.

      • Your neurologist told me and the MS Society that there was no data that could be searched to address your obvous question, hence the need for a trial…are they telling porkies?

        • And the trial is likely to cost bhillions over period of 15 years. Errr wait a minute why not check the patient list who happen to have ms, and happen to be taking this drug. So clinic 7000. 700 would have diabetes. Of which 400 are taking pioglitazone. And see if their edss scores are on average better. Yes you are right thats just crazy. We need to do a multi billion placebo blinded trial over 3 phases. Phase 1 let’s check if pioglitazone is safe for subset of population who are in the clinical trial. 15 years later we may have parabolic effect where drug st highest efficacy works less than st a lower efficacy. Then fudge the data set to get approved by fda and Ema with plenty of sweetners under the table. Fudge the formula slightly to make the side effects less and rebrand it at a 1000 times inflation.

          • Let me rephrase with less aggressive tone. The heart my beef is the following. For a new chemical and biological entity that never existed I agree the gold standard should apply. Therefore 3 phase trial to establish safety and efficacy over 15 years. There are no short cuts. But for a drug that existed over decades has been proven to be safe, really requires a multi billion trail? Doesn’t it sound nonesencial? I understand why pharma promotes this approach. To repupose existing drugs requires just on phase study, formal or informal where people are given the medication then using off the self statistical tools to check efficacy from the primary and 2nd endpoints. The cost of the trial is cost of medicine and admin people. Why is this approach wrong? Give me counter reason that breaks my logic. I will gladly modify my views.

          • The metformin trials trials were being funded by the MS Society….post COVID-19 it remains to be seen what will get funded and what will not.

            Some of the people who were in the driving seat will not be there when things re open.

            As for the pioglitizone we know what trial we want to do, there is anecdote already.

      • MD,

        “Pioglitizone has been on our radar for some time and Prof Mahad had supplied us with an early peak at the data, we know how to use it to get best target smouldering MS. Wish us luck.”

        I do wish you and all MS research labs good luck. Tackling progressive MS / worsening disability is what I’d like to see addressed. I’m a happy bunny at the moment – Arsenal won the FA cup, but a bit sad at the value of my BT shares. Take MD2 for a nice pint this evening at the Punch House or the Brewery Tap. If I ever see you strolling along the river Lea I’ll say hello. With Prof G on his hols you should get out in the sun and enjoy the summer.

  • Ofatumumab , B cells , Stephen Hauser and more is more aproach 🙂

    Drug prevents multiple sclerosis relapses in phase 3 trial

    https://medicalxpress.com/news/2020-08-drug-multiple-sclerosis-relapses-phase.html

    Based on what has been learned so far, and encouraged by the partial success of ocrelizumab in treating progression, Hauser and UCSF colleagues aim to explore whether even stronger, but still safe, dosages of anti-CD20 medications given at the time of diagnosis might permanently stop progression of MS and the degeneration of neurons, effectively providing a cure. In addition to anti-CD20 therapies, a variety of other approaches are also now being explored to eliminate culprit B cells in MS even more effectively.

    “While there is not yet a cure, a generation ago MS patients typically became cane- or crutch-dependent within 15 or 20 years, but now they often are spared from significant disability,” Hauser said. “The improvement in MS treatment, especially with drugs that specifically target B cells, is one of the great success stories of medicine.”

    A serio?

  • Does anyone know what has happened to the Vitamin D Council – the non-profit one based in the USA, which was full of good and well researched info and articles on Vit D – collated and in some cases written by Dr John Cannell. The website appears to be non-existent and all of my saved bookmark just bring up error messages………

  • Reading the BMJ I came across an article about ‘doctors refuse to speak to someone lower in the hierarchy’. Article named ‘How hierarchical communication “rules” hamper doctor training and patient care.’

    I can’t imagine Barts Blog/ Barts MS staff being like this and it is one reason why this blog is so fantastic, you seem approachable to pwMS and staff and I am very grateful for that.

    Ta very much.

          • Reading about it more, disrespectful behaviour to other staff members is ingrained in healthcare. This is so sad to hear and how it can jepodise patient care.

            One idea that is discussed is to have mandatory training for all hospital staff, that covers how disrespectful behaviour impacts negatively on patient care. Surely a doc that is disrespectful to other staff is doing harm to patients ultimately.
            I wonder are there any staff like this caring for pwMS? Not meaning at Barts but elsewhere. Food for thought…..

      • Just read Hans Christian Anderson if you want to read fairy tales…We invented most of the arrow heads and this is a shaft with no tips. There is so much wishful thinking about this. The idea that cannainoids are going to have a major effect on the immune response is fantasy…They are not good enough. Neuroprotection in MS. The trial design is rather rubbish, symptomatic control possible but not really happening…….drugs against the re-uptake mechanism is fantasy as there is no specific reuptake molecule, FAAH inhibitors are largely dead meat since the failed phase I trial was killing people the only option seems to by MAG Lipase inhitiors.

  • Hi all,
    In my research I came across a video (already 7 years old) ( https://www.youtube.com/watch?v=iMycnR3ROQo&t=1362s) from Prof Volmer explaining, among others, the concept of neurological reserve and explaining PPMS. First I was surprised to learn that only 5 to 10% of leasions create a relapse so most are subclinical. Second PPMS would in essence have the same biology as SPMS but without prior RRMS which I know from reading this blog this team also believes it is all the same disease. But I found it interseting the way Prof Vomer discribed that is essence going straight to PPMS is actually a matter of statistical un-luck. The reasoning would be that with on average 10 new leasons per year and only 5 to 10% chance of being on a critial pathway and giving a relapse, over 30 years 10 to 15% will never have a relapse but accumulate the same brain damage until they lost their neurological reserve and go progressive. It makes sence I think…

  • I have been in the hospital without a phone and just recently got it back, so I don’t know if my question is too late.

    I saw the news today about early treatment of inflammation in first five years in reducing neuronal/axonal damage and progression to degeneration. There are also many studies and trials of remyelination therapies right now as well. If there were a way right now to induce remyelination in the CNS, would it even matter or have any effect on gray matter that has already started to degenerate?

    Thank you for your time.

  • Just wanted to say that I really enjoyed the Mendelian randomisation study paper posted by Prof G on Twitter.
    https://academic.oup.com/braincomms/advance-article/doi/10.1093/braincomms/fcaa119/5892761?guestAccessKey=9d08a0b7-393a-4818-ac08-e570ba7beb23

    I saw a virtual lecture yesterday on familial hypercholesterolaemia including how Mendelian randomisation led to the identification of targets and in 2 years had a siRNA drug in a clinical trial… and I thought I really need to get my head around Mendelian randomisation studies, now I have a really good reason to find the time to do this!

  • I was diagnosed 2 years ago and I am 48. I started on Tysabri and so far NEDA. I have small bladder issues, but other that that no symptoms. I jog three miles a day and work full time in technology. I have spinal lesions from C1 – C 7 and the report says mild diffuse. My neurologist says I will probably need a cane in 10 years. I know spinal lesions typically have a worse outcome, but in your experience does everyone with them end up needing a cane? Is there a possibility I will be able to walk unassisted?

  • WHERE THE HELL IS PROF G?

    I’m not being rude, but Prof G had a nice luxury holiday in the south west of England (I doubt he stayed at Butlins), should be fully rested and energised, and has gone AWOL! I pay good money to access this site and feel short changed. It’s like Ant without Dec, Morecambe without Wise… no wonder MD feels near death’s door – he’s been treated like a pack horse while Prof G puts his feed up. T4TD should be T4TM (month). Whatever they’re paying you MD it’s not enough. I’m guessing Prof G is sulking because ECTRIMS ACTRIMS is virtual so no air miles or freebies from pharma.

    • Luis, the last link you posted is really interesting: the concrete use of theophylline for promoting myelization in CNS. I’d love to hear the view of Barts about this strategy…

      • I agree, really interesting. Theophylline is structurally very similar to caffeine, does caffeine have a similar effect?

        • See below…and their you hit the nail on the head…we are a nation of tea drinkers yet we are MS central does the tea stop the MS, I think I can say if it has an effect it does not do a good enoug job.

      • Before reading this I thought “cure of the week”…we have this every few days when their is “ground breaking” news and surprised the headline is not drink tea, save a nerve…earlier on this week there was a post cashew nuts do the same. Their is a compound in tea called theophylline which promotese myelination in old and young mice. The science is all supper sexy and could it lead to a treatment? I don’t know but I havent got the time to do this paper, it could take hours to do it justise but even if it is true it will be years before it would be a treatment. First I look at the target and I can see EEF1A1 (the target) is every where and at high levels so it will not be a sensible druggable target as it would have side eefects. Theophylline hits it and this is used in COPD (obstructuve airway disease) in humans. The dose is 600mg so tha is about 10mg/kg used in the mouse study. However in the toxin model you do nothing and it repairs these agents speed the process.

        Remyelination of the peripheral and central nervous systems (PNS and CNS, respectively) is a prerequisite for functional recovery after lesion. However, this process is not always optimal and becomes inefficient in the course of multiple sclerosis. Here we show that, when acetylated, eukaryotic elongation factor 1A1 (eEF1A1) negatively regulates (inhibits) PNS and CNS remyelination. Acetylated eEF1A1 (Ac-eEF1A1) translocates into the nucleus of myelinating cells where it binds to Sox10, a key transcription factor for PNS and CNS myelination and remyelination, to drag Sox10 out of the nucleus. We show that the lysine acetyltransferase Tip60 acetylates eEF1A1, whereas the histone deacetylase HDAC2 deacetylates eEF1A1. Promoting eEF1A1 deacetylation maintains the activation of Sox10 target genes and increases PNS and CNS remyelination efficiency. Taken together, these data identify a major mechanism of Sox10 regulation, which appears promising for future translational studies on PNS and CNS remyelination.

        So there you have it they use something that is every where to affect Sox-10 which is restricted to oligodendrocytes but to explain this properly will take agains, I am sure that people will reach to the drug cabinent and I can tell you theophylline will do nowhere fast..I will pass on this one and will watch this space for the next fifteen years to see where it moves. Sadly even if this is the best thing since sliced bread there is no sure fire way to test it multiple sclerosis would noy be the logical place to start

  • Yes , very interesting indeed. Guillain Barre Syndrome is a disease of the peripheral nervous system where it is believed that the symptoms manifest as a result of demyelination of the nerves. Treatment is usually 6 successive doses of immunoglobulins delivered critically 24 hours apart for 6 days followed by, maybe, 4 weeks on life support then 8 weeks of intensive physiotherapy rehab. Under such a regime the nerves are given the opportunity to remyelinate and best case scenario is complete recovery. To get a parallel result in the central nervous system using theophylline would be absolutely amazing !

  • New blood, new hope: Transfusions protect the brain from stroke damage

    https://medicalxpress.com/news/2020-08-blood-transfusions-brain.html

    “The idea is to change the immune response that happens after stroke,” Simpkins said.

    “The immune system doesn’t recognize much of what’s happening when there’s a stroke,” Simpkins said. “So the neutrophils go to the brain and try to clean up the damage that happens. But there’s too much in the brain and those same neutrophils release MMP-9, which then exacerbates the damage.

    “What we learn is that stroke is simply not a cerebral vascular event. It’s a whole-body event. Both the brain and the body get signals that something’s going on in the brain and as the immune system responds to try to help, it actually worsens the outcome. Therefore, by removing the blood and replacing it with the blood of those that have not experienced stroke, we get good outcomes.”

    Could this be use in ms???? one day???

  • Well this fit nice in what Doc Mouse has been saying all along

    You have to look for the cars in the highways but also in the parking lots and garages

    Host tissue T cells may have an unexpected role in graft-versus-host disease

    https://medicalxpress.com/news/2020-08-host-tissue-cells-unexpected-role.html

    “This study is an example of how we must never assume we know everything about disease mechanism and must always be willing to challenge prevailing paradigms if that’s where the data leads.”

    🙂

    • And a Brutons Tyrosine kinasethat inhibits B cells (and macrophages) is approved treatment for Graft versese host disease. f the conditioning can’t clear out the skine what is the chance it does much in the brain.

      • Rituximab can gets the b cells from the garage 🙂

        Conclusion: RTX depletes lymph-node resident B-cells as
        efficiently as circulating B-cells, suggesting that lymphnodes
        do not constitute a RTX-resistant environment in
        humans. As lymph-nodes contain AQP4-specific B-cells,
        this depletion may be a mechanism by which RTX shows
        clinical efficacy without reducing AQP4-antibody levels.

        Conclusion: RTX depletes lymph-node resident B-cells as
        efficiently as circulating B-cells, suggesting that lymphnodes
        do not constitute a RTX-resistant environment in
        humans. As lymph-nodes contain AQP4-specific B-cells,
        this depletion may be a mechanism by which RTX shows
        clinical efficacy without reducing AQP4-antibody levels.

  • It was mentioned today on a few news websites, that there is now a new blood test to check for gluten sensitivity and the endoscopy procedure might not be required for diagnosis.

    I wonder if this is useful for pwMS? as several pwMS report feeling better on a gluten free diet.

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