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  • I have heard about a new targeted drug treatment for CoVID-19. The Australian news article talked about the ability of this new drug therapy be tailored to any virus and it will be ready for clinical use within 2 years. It was a bit sketchy on specifics. (https://youtu.be/y0mPqsno4z8). Applying this to MS, it could be adapted to EBV and Gavin’s favourite, the HERVs? Maybe one for Michael Pender?

    • One way to start a properly powered trial is through crowdfunding if enough of us team up to fund an antiretroviral trial targeting EBV it could be possible but we need a few people ready to team up and help fund it. A phase 2 trial would be enough to attract the ms scientific community once we get a positive readout from that trial. The cost would be between 2-5 million for a phase 2 trial involving 150-300 people so it seems like a big number at first but lets break it down to something more easily achievable. Let’s say this trial costs 3 million. We would need 1000 people giving 3000 $ or have 5000 people giving 600 $. Now all of this seems big however in the grand scheme of things its not that much, the National MS Society got 193 million in 2019 and 191 million in 2018. In this scenario we only need 3 million. Also the MS Society of Canada during that time had 50 million a year but after the costs of planning events and services to people affected by MS gives about 10 million in research every year. Therefore I do think its achievable if we all team up together and the 3 million could be less than that if one of the MS societies would be interested in funding only part of the trial like simvastatin or lipoic acid and others that they have funded in the past. Another way would be to get a pharmaceutical company to help out either by funding it completely or partially through giving their medication for free during the duration of the trial. In terms of funding strategies their are many different ways of achieving this which I could go into more detail.

      • One way to start a properly powered trial is through crowdfunding …..£2-4,000,000 is alot to crowdfund

    • It will be ready for clinical use within 2 years.
      We will have forgotten about covid by then…..:-)

      • 18 months ago there were 2-3 month predictions. I suspect CoVID is still going to be the subject of discussion, much like HIV, for decades to come. It won’t be so feared and there will be better treatments, but it’ll cause small outbreaks and there will be a push to vaccinate against the next strain. Hopefully, evolutionary pressure will have reduced the anti-vaxxer sentiment.

  • Hi, is it possible that during Ocrevus treatment if there is an infection, the PlasmaBlasts and Plasmacells are on rise (or any of cd19 B cells which are not affected by OCR), which then when blood sample is taken, CD19+ gives higher percentage?

    • I have seen alemtuzumab data where there are more frequent bloods and if there is an infection cell number can shoot up. There are few plasma cells in the blood and plasmablasts and plasma cells are not killed by ocrelizumab

      • This is great idea what you proposed. Generally plasmablasts and plasma cells are inside lymph nodes and if there is an infection they cross into blood stream? Can I imagine it like that?

  • I take Ocrevus, and I’m scheduled to attend in-person classes in a month. My University does not require students to take the vaccine. I requested a letter of accommodation from my neurologist, asking the university to record lectures for me (so I could avoid classes), but she was unwilling to provide it.

    I’m in my 30s, I deal with Afib, and high cholesterol, though I’m reasonably fit.

    How concerned should I be?

    • I guess most students want to go on holiday go to concerts football matches and so are getting the jab and importantly age is is on your side. However, our unversity was recording lectures years before the pandemic so just write to them and ask if they do this. I suspect you will have T cell response from vaccine

    • I feel that apprehension. For what it is worth, in my opinion I think it is very disappointing that your neurologist wouldn’t write a letter for accommodation. Have you considered requesting a test to see where your B cell levels are? In the context of current pandemic circumstances, perhaps you are one of the “lucky” ones that have a faster repopulation of B cells. If that is the case you can discuss with your neurologist about whether a booster shot before your next Ocrevus infusion is appropriate. To be clear I don’t know if such course of action is appropriate but it is something I have been contemplating.

  • I came across the Phase 3 results of the Ublituximab trials. It’s another CD20 depleter but the results look impressive in respect of relapses. Any thoughts on how it compares with the other CD20 therapies?


    I watched a couple of recent short videos by Profs Steinman and Hauser. Both supported early highly effective time therapies and both identified a need to get rid of plasma cells in the CNS – looks like lots of team are singing from the same hymn sheet. They also mentioned plasmablasts. Will these be targeted in the Sizomus study?

    • There isn’t a bandwagon that old Larry hasn’t eagerly jumped on 😉
      Glad we were well ahead of the curve on this but expect we’ll be quietly airbrushed out of the picture over time.

    • They (e.g. prof steinman in a recent video) are singing the praise of of ublixtuximab as the first agent to get relapses below 0.1 = 1 relapse in ten years, however the comparitor was less than 2 relapses in ten years and the comparitor was teriflunomide. Now this is better that alemtuzumab was in its pivotal trial. Do we think teriflunomide is more active than alemtuzumab at stopping relapses? So the group of people in the trial were less active, this is not surprising because if you were highly-active would you want the risk of being on teriflunomide? Maybe the neuros should be asking why we are still doing this? A non-inferiority (not worse than) trial against ocrelizumab would be the most ethical way to go but it is not the most commercial way to go as it is risky in case ocrelizumab is better…using teriflunomide, which we know is not effective for many people and simply removes brain reserve in the people where it fails. People obviously think that early treatment is good because we are having a trial of anti-CD20 against beta interferon, glatiramer acetate, teriflunomide, or dimethyl fumarate and I believe Dr. Ben from Barts is part of the Team…wonder how many referrals he will get?

      We will now have three and a bit anti-CD20 one fully human (ofatumumab), one humanizised (ofatumumab) and in terms of COVID-19 two demonized (ocrelizumab and rituximab because they blunt vacines) and now a chimeric half mouse and half human but with low sugar content on the tail to make it a better cell killer from Natural killer cells…How many of those get in the brain during MS?. It is an infusion (1h) that is quicker than ocrelizumab (2-3h) but as it is 6 monthly dosing does this matter much, your day is no doubt wasted by having an infusion? lasting 60 or 120 minutes. However now something they have not mentioned at all and this is anti drug antibodies, we know that rituximab caused people to make anti drug antibodies (up to 35-40%) how many does ublixituximab cause. Dr Angry is on the case:-) Why they didnt at least humanise it I dont know. Next I have yet to see the repopulation kinetics but they are using 450mg

      They apparently plan to undercut ocrelizumab and ofatumumab on price.

      The results of this study are online

      • Spot on, to me as patient it matters little if semi annual infusion is 1 or 5 hours. Whether or not it makes a major difference to hospitals, not sure. You could probably schedule two or three patients this way but it’s unclear to me whether beds is a real bottle neck. Last time I was there it seemed fairly quiet so maybe not.

  • Has there been much work into anti histamines in MS. (Not Clemestine)

    I mean, maybe to cool the inflammatory response in some way?

    I know anti histamines are used against allergens, I just didn’t know if it slowed any immune response to whatever our immune system is responding to.

  • Any thoughts please on vaccine response while undergoing cladribine therapy (just started year one)? Having had the covid jabs while on fingolimod, does what protection I may have had now wane further because my immune system is being reset? Secondly, will further jabs within the 24 month treatment period work at all or will it be as was with fingolimod? Finally, are both these issues the same for a friend shortly to be starting alem?

    • Fingolimod will have blunted your response and going onto cladribine may not influence that much but we dont know the T cell effect on fingolimod or cladribine. The booster jabs should work . Same issues with alem I suspect

  • Mouse Doc- Early in my MS career (like 30 years ago, almost, now), I had Optic Neuritis several times, at least one full blown in one eye, and another bout which was kind of drawn out over several+ months in the other eye. (There was more of this to a lesser degree, early on.) Everything A-OK now, with the eyes, which brings up the question… Even back then, “they” knew that optic neuritis was not something that usually persisted, either symptomatically or returning in “bouts”. So “doc”,- how come? Only makes sense to wonder why this doesn’t return later in one’s MS career, and then to try to extrapolate into a treatment or causal explanation that could be applied to other MS situations? Would be nice if everything else kind of “faded away” also. Why do optic bouts with MS usually cease while vision returns close to or at normal and remains there? 🙂

    • In all nervous pathways there is reserve and this is true of the eye too so youu can loose nerves and the brain compensates

      • Yes (?), but…I (and I suggest others as well) do not experience continuing relapses of Optic Neuritis after the first few years in the relapse phase of MS, or slow vision deterioration in the later progressive years. At least not a noticeable amount, compared to say, leg strength or bladder function. Also, it sounds then, that you are suggesting the reserve in the optic pathway is HUGE as compared to other nerve pathways such that damage in the optic pathways can never amount to enough to make a significant difference. I still wonder about my initial observation. I’m sure many wish their legs and bladder held up as well as their eyes do.

          • The optic system continues to be affected it is is being monitored as a surrogate for progression.

  • I know there’s no data, but what’s the view on one or two boosters for mRNA vaccinated B-cell depleted population?

    If one was to go this route, would boosters optimally be the same or a different vaccine?

    • Boosters will come there is data on switching AZ to pfizer and the other way round…it needs to be published

      • Good to hear. Now if Swissmedic only approved AZ… 🙂

        Right now it looks more like more Pfizer or switch to Moderna for me….

        • Moderna give a higher response than pfizer so this would be my choice. Pfizer give more response than AZ. Perhaps what we need is the variant vaccine

  • The blog focuses a lot on the brain (lesions, atrophy etc) and as a reader i am assuming that the same principles apply to the spinal cord. However, when considering treatment options should evidence of spinal disease not be a prominent factor. For instance, we know that alemtuzumab and HSCT have the greatest impact on brain atrophy (and i assume therefore spinal cord atrophy) but anti CD20s perform better than alemtuzumab when it comes to controlling relapses. Given that a spinal relapse can have dire consequences, should a patient with spinal disease does this not tip the balance a little for the patient with spinal disease i.e. to focus on relapses more?

    • > anti CD20s perform better than alemtuzumab when it comes to controlling relapses.

      Is this even true? I would say alemtuzumab wipes out everything ocrelizumab wipes out plus a bunch more stuff, so it doesn’t make sense that it would be less effective at controlling relapses… If there is indeed data suggesting that, my guess is it’s influenced by the fact that alemtuzumab has been relegated mainly to use as a second- or third-line therapy in people who have breakthrough disease activity on another drug, whereas ocrelizumab is being given to tons of people first-line, thus the alemtuzumab population probably has a higher proportion of people with more aggressive disease.

      • Hello,

        Could you please share the links to them? I was unable to find any study on cladribine or rituximab in which the brain atorphy was even close to the brain atrophy rate achieved with use of alemtuzumab (apart from the CIS cladribine study).


        • We just heard from Frederik Piehl at our MS meeting that in their Swedish cohort the brain volume loss on rituximab was greater than the interferon-beta treated comparator group. The BVL data in general on anti-CD20 therapies is very disappointing. Anti-CD20 may be good at stopping relapses and MRI activity but is not that effective at stopping smouldering pathology or the real MS.

          • Ouch, that is really disappointing… I wonder if the BVL may actually differ in pwMS treated with rituximab vs treated with ocrelizumab, in the 5 year Roche trial, the BVL ocrelizumab ratio was shown to be “better” then BVL Rebif ratio. Is it actually a coincidence or is ocrevus superior to rituximab in slowing down the brain atrophy? Or maybe is it strongly dose dependant, as ocrevus is much more potent compared to the same dose of rituximab?


          • One more thing – is there any data on PIRA in use of Alemtuzumab? I was looking for it, but couldn’t find data on that in the widely available studies or articles. Thank you in advance! 🙂


          • Much lower rates than with the other DMTs; in fact, most patients in the CARE-MS trials treated with alemtuzumab stabilised or improved.

          • Well, if we look at it in that way – most of the people in Ocrevus 5-year trial stabilised or improved, “only” ~18% worsened, 90% of these 18% worsened due to PIRA but it is as well safe to say that most of the people stabilised or improved in terms of CDW.

            At 12 years follow up for Alemtuzumab 31% people worsened, also almost 50% (48 out of 108 participants) discontinued the screening throughout the whole 12 years, so who knows what the real number is. What is the most interesting is how much of that 31% CDW was due to PIRA, was it 15% or 90% of that like in the case of Ocrelizumab, that number changes the whole outcome.



          • Was this a side by side comparison for patients placed on either DMD at the same point in their MS journey, with no other DMDs or lack of treatment in the mix at any time? I was on Ocrevus 3 years ago, but after 34+ years of MS at the time, and paraplegia, heading to tetraplegia, with no attacks for the prior 10 years, it was completely useless for me and I stopped it.

  • Would there be any benefit in a joint trail of neuro protectants between all brain illness charities, I know there all different illnesses with different mechanisms that cause damage etc.

    But could it be possible that something may benefit all. If they joined up on a trial. Rather than being fragmented. Could it get somewhere


    Could there be something out there that’s already available,

    funded by all the charity’s, therefore make a bigger impact. Something similar to the octopus trial? Maybe it’s a long shot.

  • I started Tysabri a couple years ago and since have had three dysplastic nevus removed. Is melanoma associated with Tysabri?

    • there are a few papers Kelm RC, Hagstrom EL, Mathieu RJ, Orrell KA, Serrano L, Mueller KA, Laumann AE, West DP, Nardone B. Melanoma subsequent to natalizumab exposure: A report from the RADAR (Research on Adverse Drug events And Reports) program. J Am Acad Dermatol. 2019 Mar;80(3):820-821. doi: 10.1016/j.jaad.2018.10.052.

      However “Collectively, these results further support that natalizumab therapy does not increase the risk for nevus transformation and that natalizumab exerts anti-invasive and antimigratory activities in vitro. Because these capabilities of malignant cells correlate with their metastatic potency, our findings provide evidence that natalizumab might have a protective effect on melanoma development and give reassuring data for its use in treatment of MS”.

  • I understand data on response to anti-Covid19 vaccines in terms of antibodies and T-cells on people on Anti-CD20 DMTs such as Ocrevus. I wonder whether in the meantime we have data on cases of reinfection among people on Ocrelizumab (and/or other b-cell depleting DMTs)^ after the vaccine? That may help infer whether the vaccine works, regardless of the development of detectable antibodies… Thanks!!

    • Good question the rate of re-infection is about 1 in 1000 and I think from the registries we have only heard about 1000 people getting infected so if one gets re-infected what does it tell us. Yesterday I heard of reports of two people being infected after vaccination both did OK

  • Regardless of radiological findings, is it generally assumed Ocrevus is failing if the user consistently sees CD19 values of around 2.0% prior to each biannual infusion? Or, perhaps, should CD27 instead be reviewed and if the value is below .05% all is to be considered going fairly well?

    PS. I made Covid antibodies from Pfizer vax w/ shot at 4 months post infusion. Hooray.

  • I would appreciate any theories as to not “recovering” from the expected temporary setback after Ocrelizumab infusion.

    Anecdotally, some pwMS, myself included, experience a near immediate and abrupt decline post infusion, but with excellent MRI findings in regards to WML.

    Most seem to at least stabilize, while a small subset of those infused with Ocrevus feel absolutely wretched. Frustrating since the side effect profile of Ocrelizumab is promoted as primarily being limited to infusion reactions.

    I understand the theory of MS actually consisting of separate distinct disease pathologies, or a combination thereof, which I presume holds some explanation. Curious though, why this B cell therapy could amplify Sx of those in which the arrow was shot at the wrong target.

    • Infusion related reactions are common place with alemtuzumab and this is why steroids are given it seems that existing lesions are affected

  • so, if someone had their first covid vac in Feb, Ocrevus 4 weeks later, then 2nd vac 8 weeks after that….would the talk of this booster which is going to be started given in September, which just happens to be when next Ocrevus is, be of any use to that person?………………………………………………………………………….
    Or is it that they will generate some small kind of immune response and something is better than nothing?

    Two thirds of Ocrevus users are not really generating any response to 2 vacs anyway it seems, so why would a third be any different?

    • You make a good point and I agree it may not be of value so I think we need to collate available results and optimise if this is feasible.

      • Hence the idea of waiting for B cell repopulation using a bridge of some DMT, say Natalizumab, in an efffort to hopefully slow disease progression. Then boost or completely revaccinate. Interestingly, with the notion of B cells being a driver of MS, it makes me wonder why a 6 month infusion cycle is recommended where it could be ~5.5 to 3 years for B cell repopulation. Would it not be more cost effective to test the patient and when there is evidence of repopulation, the infusion resumes?

        Going back to the idea of a switch from Ocrevus to Natalizumab, is it true that Ocrevus renders the JVC test unreliable thus increasing risk for PML since you wouldn’t know your JCV status? How can one make the switch with less risk?

        • I’m not using ocrevus, so I’m not into the details, but do I understand you correctly that the 6 month infusion is given no matter what – regardless of B cell repopulation?
          I thought (naively) that 6 months was the average, and that prior to new infusions, B cell levels were tested to determine whether new depletion was in order.
          If you deplete no matter the current level of B (and T) cells, it seems to me you will have some cases of serious overkill…

  • A few questions I had from the June post
    Can we get more information on the effects of MS and the PNS?

    Also was wondering, if you have interns running around, updating the MS article page might be a good idea as the moderators have mentioned its a high-view article that is out of date.

    MD said and I quote “ProfG is not that bashful as he did tweet his meat and two veg:-)”. Can we get some context for science??????

    • Prof G had had his accident no doubt have some serious pain meds and in haste to show x ray of the pelvis screws…soft tissue got another meaning:-)

      No there are no interns running around

  • Does anyone have an opinion that they can share about IVIG in general for people who have MS?

    I’m curious about it since I haven’t had ocrevus in over a year because I had a horrible reaction to it. I know a lot of people really like it, but having 3 infusions of that turned to be a real disaster for me.
    My B cells are still at 0.

  • I was refused entry to Sizomus trial because of a possible (pretty unlikely) drug interaction with another medicine I take. I presume this was mainly because Sizomus is a Phase 1b trial and they don’t want to get black marks at this stage. Bitterly disappointing because I was refused access to alemtuzumab for four years because of a phantom worry on my consultant’s part.

    Do you have any idea of when, if this trial goes well, it might enter Phase II? Time and brain are a-wasting

    • Sorry to hear this, but as you say if something happens it may mean there is no phase II. The first part is complete the second part phase Ia/IIa. Then it is up to Takeda…do they do the next step or flog-it to someone else

  • Hi, thanks for the monthly Q&A: I’d like to ask if allergies management is important in MS. I’m allergic to pollen and mites, and possibly more, and I’d like to pursue allergen immunotherapy. Currently on natalizumab. Would it be a good idea?

  • What do you think to the NHS and the government, giving away and selling access to everyone’s medical records?

    Not a lot of people know this. As it’s not really on the news. A little bit under the radar. In the middle of a ‘pandemic’

    • I dont know…depletion of psoriasis B regulatory cells:-)…In the examples you report there is worsening with time

      • Thanks MD. For me the skin anomalies started to show up after the second Ocrelizumab infusion (5 month ago). I’m taking my second Pfizer jab this Friday, and third Ocrelizumab dose end of the month.

        Had to start phototherapy today as one of the guttate appeared on my forehead, fingers crossed psoriasis stop expanding.

  • I am 49 and for years doctors always asked me if I was an athlete because of my low heart rate – 50. I do jog everyday and do a weight lifting boot camp three days a week, but I am no elite athlete. I was diagnosed with MS two years ago, although I am sure I had it for many years. I did some research and it sounds like MS can cause bradycardia. Should I be worried and make a bigger deal about it with my doctor?

    • Sounds like your fit and healthy and have a low resting heart rate. Baring any QtC prolongation, I wouldn’t overthink it. If your really worried, see a cardiologist.

  • I recently came across this clinical trial: https://clinicaltrials.gov/ct2/show/NCT04025554 (Anakinra for the Treatment of Chronically Inflamed White Matter Lesions in Multiple Sclerosis). I assume they are referring to SELs when they say “chronically inflamed white matter lesions.” Do you have any thoughts about how promising this drug may be for tackling some aspect of smoldering MS?

  • After 2 months of teriflunomide, my B-cells have decreased by 40% (while ALC remains unchanged).
    Evidently, teriflunomide is supposed to affect B cells, but I haven’t been able to find in the literature what % of reduction in B cells is ‘average’ or ‘desirable’.
    If someone could comment on this?

    • In some cases the absolute number go down but the percentage don’t change. It depends on the type to determine the importance

      • The absolute number of CD19 cells went down from 120 to 71 (so a reduction by 40% in 2 months).

        • I can not provide any literature, only my experience….after stopping TERI, my circulating CD19 b-cells increase by about 40%.

          • thank you for this information – the reason you stopped had nothing to do with your CD19 cell reduction?

  • May I ask how do Memory B cells work against an antigen? After activated it will replicate and some class change to Plasma cells and some presenting to T-cells via T help?

    In the case of autoimmune, what could the triggers of activation of Memory B cells be? The antigen is always there….

    Thank you!

  • Any possibility some Covid variants aren’t being picked up on Covid rapid or pcr tests? I’ve caught two significantly severe colds since early May but tested negative. I go out rarely, always with N95 mask, but family members must go to work and school and brought home cold. Family members tested negative too. I don’t want to wear a mask inside my own home but the ease and swiftness of transmission of these “benign” colds is getting me to question my safety from Delta expected to become dominant in my area in next few weeks. A bit anxious.

    • Not very helpful to be honest. His suggestions are basically vitamin D (we know), IV vitamin C (smacks of naturopathy and I think someone would have noticed by now if this made a significant difference), quercetin (maybe, I don’t think many people with MS have tried this one; apart from EBV effects there is also some evidence it may have senolytic properties which could address one aspect of smoldering), olive oil, and coconut oil.

      This paper from a cancer research journal has a much larger list of potentially helpful anti-EBV compounds:


      Also there was this small, positive phase II trial of andrographolide in non-active SPMS. Andrographolide does inhibit EBV in vitro although I don’t think they discuss this in the paper:


  • I find these MS blog articles so incredibly helpful. The only downside is that I’m finding it rather tricky to keep on top of them all with all the comments to read as well! To avoid information overload for folk with MS and hopefully save contributors precious time, please can I suggest that there are maybe only a maximum of two per week? What a lifeline this blog has been – haven’t seen a neurologist for two years. Thank you, thank you, thankyou!

  • “thank you for this information – the reason you stopped had nothing to do with your CD19 cell reduction?”…….correct, the CD19 reduction, or rather the immune modulation, is exactly why I was using TERI. I was on OCR and wanted to keep my CD19 low, so I decided to use TERI while I transition to CLAD. TERI effectively keep my CD19 below pre-OCR baseline, but when I stopped TERI my CD19 jumped from 50 u/l to 93 u/l, over a three month timeframe. Stopped TERI due to adverse side effects.

  • I was thinking of the DODO study… if one gets double ocrelizumab dose its higher concentration effect will last only for one half life. Wouldn’t it be worth to see if dosing every half life has better effect? One would have higher ocrelizumab blood concentration for a longer time than with standard and dodo dosing schedule.

  • Assuming that the theory of EBV as an important factor in MS and its elimination could lead to a likely “cure” of MS, or a very significant reduction in disease activity, what is the predicted effect of this on brain atrophy? Are there any suspicions about the effect of using Ocrelizumab in combination with TAF (tenofovir alafenamide) on brain atrophy? The question is dictated by the fact that such a clinical trial is currently being prepared. Are there any grounds for assuming that it is the presence of EBV that causes the accelerated brain atrophy? Are there any indications that the use of ocrelizumab with TAF may result in stopping the atrophy caused by MS? Is there any connection between microglia and EBV?

    Given the negligible effect of anti-CD20 therapy on brain atrophy, wouldn’t it be a better idea to use Alemtuzumab in such combination therapy?

      • Not sure what is considered as the “early” but in the main Ocrevus trial, the mean duration since the onset of MS symptoms was 6.1 years in the placebo group and 6.7 in the ocrelizumab group. Is 6 years considered early or late?

        • Yes, I am aware of that, though according to the blog posts, alemtuzumab does “something to the brain atrophy” which is not yet fully explained, understood. So does it really do something unusual to the brain atrophy or is it just a matter of the difference between time since disease onset in between these two studies?

          • Until proven otherwise I believe it is an issue of time cladribine 9 years rate is 0.6 cladribine before MS diagnosis is 0.15 I have seen 0.18 for rituximab too.

    • Actually I think Zidovudine ( known to inhibit EBV replication ) in a proper concentration would probably be enough as a mono therapy to be highly successful in a clinical trial setting for all forms of MS. The reasoning for this is that Zidovudine crosses the blood brain barrier but TAF does not really cross the blood brain barrier.

      • I couldn’t find much about whether TAF is bbb penetrant or not, and if it is – what are it’s concentration levels.

        Though there is an interesting research about CSF/BBB/NfL with use of TAF:

        Our hypothesis prior to initiation of the study was that switching from TDF to TAF could pose a risk of neuronal injury due to decreased CNS exposure of tenofovir, leading to a measurable increase in plasma NfL concentrations. Unexpectedly, we found the opposite: a small, but statistically significant, decrease in plasma NfL in the group receiving TAF 84 weeks after the switch. CSF tenofovir concentrations are six times lower when administered as TAF compared to TDF [31, 32], but since CSF concentrations do not correlate with intracellular concentrations [33, 34], the levels in macrophages and microglia were most likely high enough to have sufficient antiretroviral effect and prevent an increase in HIV-related CNS injury.

        The mechanisms behind the reduction in plasma NfL 84 weeks after changing from TDF to TAF are unclear. One possible explanation could be the increased intracellular concentrations of tenofovir DP in macrophages and possibly microglia with TAF as compared to TDF, which may contribute to reduced neuronal injury through better virological suppression [24, 35]. There is, however, no evidence of insufficient inhibition of CNS viral replication in patients on ART and suppressed plasma and CSF viral load, and treatment intensification does not decrease CNS viral replication or immune activation [36, 37].

        A second possible explanation could be that high plasma tenofovir concentrations associated with TDF might be more toxic to neurons than the lower concentrations from TAF treatment, and that this could increase plasma NfL levels. To our knowledge, however, there are no data regarding potential harmful effects of TDF on either CNS or peripheral neurons. TDF was not associated with neurotoxicity in a study investigating the toxicity of different antiretrovirals on rat brain cell cultures [38], nor has it been associated with a high rate of neuropathy. In addition, plasma NfL concentrations did not increase significantly during the 84-week long study period in the TDF arm, suggesting, at least, no progressive neuronal injury.

        Previous studies have shown that there are correlations between cognitive decline and renal impairment, but there are no studies on renal impairment and NfL levels [39, 40]. TAF is associated with less tubular side effects compared to TDF, especially when administered together with ritonavir or cobicistat as in this study. As a third possibility for the reduction of plasma NfL that we considered was that the improved tubular function with TAF might increase clearance of NfL or substances harmful to neurons. There was, however, no association between creatinine and NfL at baseline or follow up, speaking against increased elimination of NfL due to improved renal function in patients switching to TAF. It is unclear whether the small decrease in plasma NfL found after switch to TAF is of any clinical relevance, particularly with plasma NfL levels in both arms remaining within the limits found in HIV-negative controls.

        My question is: if tenefovir is not a BBB, how did it get into microglia?


        • Tenofovir alafenamide does not seem like the ideal candidate in terms of crossing the blood brain barrier. In what you wrote you also cited this part : “CSF tenofovir concentrations are six times lower when administered as TAF compared to TDF [31, 32]”

          So 6 times less concentration in the cerebral spinal fluid compared to tenofovir dimethyl fumarate.

          Here is also an interesting article in regards to TDF :

          Zidovudine has a median 65% penetration, although variability between patients is high.30, 35.

          In this cohort of subjects, the median concentration of tenofovir in CSF was only 5% of that in plasma, levels of penetration (CSF to plasma concentration ratio) that are much lower than those observed for the nucleoside reverse transcriptase inhibitors. Nucleoside antiretroviral drugs such as abacavir, didanosine, lamivudine and stavudine have CSF-to-plasma concentration ratios of approximately 15 – 30%.30-34 Similarly low CNS penetration of tenofovir was found in guinea pigs, who had penetration in the brain tissues of less than 5%, although CSF penetration in guinea pigs was higher than that seen in humans in this study.20 Zidovudine has a median 65% penetration, although variability between patients is high.30, 35 Tenofovir does show higher penetration than most protease inhibitors studied, with the exception of indinavir (which has lower protein binding than most protease inhibitors).36 Protease inhibitor CSF/plasma concentration ratios are usually in the range of 1% or less.37, 38 Thus, the penetration of this nucleotide agent appears to be intermediate between the penetration of protease inhibitors and nucleoside agents.

          More than three-quarters of tenofovir concentrations in the CSF were below the lowest reported tenofovir IC50 of 11.5 ng/mL.16 These low concentrations were unable to reliably suppress HIV replication in the CNS.

          The article : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299895/

          Thus I believe that we need a properly done clinical trial of a medium to high dose of zidovudine in multiple sclerosis.

          • Thank you for responding, I will definitely look more into it. Thanks a lot! 🙂

          • After reading your answer, I decided to contact the group of scientists / researchers who are responsible for reporting on the case of a patient treated with Combivir, conducting research on tenofovir alafenamide, and several other publications related to EBV in MS. I also sent them some papers and research on AZT, TAF, AZT in CSF and his ability to cross the BBB etc.

            I received the following answer:

            I think that there is no clear evidence that the drugs would have to cross the BBB to be effective in MS or that EBV is in microglia or even in the brain. AZT has quite a few side effects and is not a very effective anti-EBV treatment compared to TDF or TAF. Unfortunately we have no clinical data to support any of these choices so I would not be able to answer this question.

            The last part of the answer concerns my question why TAF was chosen and not some other antiviral drug, e.g. AZT, what is dictated by the choice of TAF, etc.

            I personally can remember that it was somehow proven that EBV is present in microglia, possibly even in astrocytes. However it was also found to be present in healthy individuals. However I am also very far from questioning the opinion of people who have been partially researching the importance of EBV in MS for the last few years.


        • Hello Lukasz,

          In your last comment you mentioned that you contacted the research group. How did you reach out to them ?

          Also, I could go into more details as to why zidovudine is an interesting compound that could be tested in a clinical trial setting.

          • Combivir is being excluded from the market as I heard today, I was talking to hepatologist, virusologist 3-4h ago, I was told that it was toxic and there are better compounds in use right now, the side effects were unpleasant. I was also told by Indian pharmacy that there are currently no drugs available on the market that contain only Zidovudine. I have found Retrovir but I was told that it is also barely available anywhere and there is no generic version of it.

            About the email contact, I would rather not post the emails here publicly. You can simply go to the specified publications, the one on Combivir in HIV naive patient or the one on TAF as lytic EBV inhibitor, these are the same authors. These researchers are from biology department of MIT, you can easily find their email contacts there or even via google.


    • Ocrelizumab has more than a negligible effect on brain atrophy, even if it doesn’t normalize it like alemtuzumab. It’s already so difficult to get neurologists to prescribe alemtuzumab that they probably think there is more chance of actually getting an intervention into the clinic if they use ocrelizumab.

      If Prof G’s hypothesis that the activated microglia and macrophages are just carrying out their normal functions in reaction to the real disease is correct, and the real disease is EBV, then anti-virals should at least stop that aspect of smouldering MS. It’s not clear to me whether there would be an immediate effect on other things like plasma cells.

  • I would be interested in knowing how much remyelination occurs for those that have taken alemtuzumab or hsct and have experienced disability improvement ( since they are still quite a few people that eventually fail these treatments ) in a 7 tesla MRI scanner.

    For example are all parts of the brain equally restored after these treatments. I would be interested because it could tell us how much remyelination occurs without the presence of inflammation and therefore tell us more about the leftover percentage that is needed for the rest of that type (demyelination) of damage to be repaired. Or if we find out that a great deal of remyelination happens without the assistance of regenerative therapies then perhaps better high efficacy cns treatments could have the double benefit of reducing relapse and further improving the average rate of disability improvement.

  • I like the fish very much 🙂

    My question this month, I wondered how common is gastroparesis caused from MS?

    My gp ruled out Ovarian stuff with scans, but I have on and off persistent symptoms that sound like it. Going to go back.. 🙁

    • I dont known but a figure of 14 in 100,000 people (general population). My MSteam.com “Up to 30 percent of people with MS report having indigestion symptoms, compared to 8 percent of the general population. Many people with multiple sclerosis (MS) experience gastroparesis, a feeling of fullness, nausea, vomiting, or abdominal pain shortly after consuming food. Women are more likely to develop gastroparesis than men.”

        • Yes thanks for statistic, I think it’s overlooked. I ‘ll discuss with my neuro next visit. But can much be done to relive symptom?

          • Hi Sue

            I know a girl with Lupus who has it and she said there are some medications (prokinetics), that can be used. Also some changes to diet, smaller meals etc

            My GP put me down for a barium swallow to see what was going on there.

  • Any thoughts on testosterone as neuroprotector?
    I realize the (pilot) studies have been few and limited, but it would seem that testosterone (and progesterone?) have some effect on remyelination.
    Do you believe this is a promising route of enquiry? And why (not)?

        • Numerous experimental studies have shown that oestrogen is neuroprotective.

          There is abundant experimental evidence that the sex hormone oestrogen might have neuroprotective actions. Observations in vivo and in vitro, as well as epidemiological studies, lend general support to this idea.

          There are several possible mechanisms to account for the neuroprotective actions of oestrogen. In the simplest scenario, oestrogen receptors, which are transcription factors, might act directly on genes that code for proteins that modulate nerve-cell survival, regulating their expression. These proteins might enhance neurotrophic support, suppress apoptosis and affect neuronal structure.

          The neuroprotective action of oestrogen could also depend on non-classical actions of this neurohormone. Indeed, oestrogen can interact with intracellular signalling pathways that are directly linked to the control of neuronal survival, such as the mitogen-activated protein kinase (MAPK) pathway, cyclic-AMP-responsive-element-binding protein (CREB) and phosphatidylinositol 3-kinase (PI3K). In addition, the chemical structure of oestrogen enables it to act as a free-radical scavenger, preventing oxidative damage.

          • Coincidence that I almost always feel closer to normal during the 2nd week of my menstrual cycle? And the other 3 weeks, the MS seems to taunt me. Hmmm…

          • Please excuse my ignorance on the topic – hasn’t oestrogen therapy been linked to an increased risk of breast cancer?

          • Oh hormone therapy is such a quagmire in my experience! Yes cancer risk for hormonal replacement therapy needs to be weighed with benefit. Estrogen/ progesterone HRT increases breast cancer risk by about 75% Estrogen-only HRT increases the risk of breast cancer after greater than 10 yearsof use. Estrogen-only HRT can increase the risk of ovarian cancer. See https://www.breastcancer.org/risk/factors/hrt . Like a lot of issues affecting the fairer sex, more studies are needed to sort out the neuro protective effects and interplay between estrogen, progesterone, prolactin, and testerone levels. I suspect amount and timing in cycle, or what stage of life – pregnant,in peri or menopause is the key. See 2019 article Impact of sex hormones on immune function and multiple sclerosis development
            ,in Immunology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6283654/.

  • Well temelimab failed to meet its primary endpoint in a phase 2 b trial. Any thoughts on this ?


    Efficacy and safety of temelimab in multiple sclerosis: Results of a randomized phase 2b and extension study


    Background: The envelope protein of human endogenous retrovirus W (HERV-W-Env) is expressed by macrophages and microglia, mediating axonal damage in chronic active MS lesions.

    Objective and methods: This phase 2, double-blind, 48-week trial in relapsing-remitting MS with 48-week extension phase assessed the efficacy and safety of temelimab; a monoclonal antibody neutralizing HERV-W-Env. The primary endpoint was the reduction of cumulative gadolinium-enhancing T1-lesions in brain magnetic resonance imaging (MRI) scans at week 24. Additional endpoints included numbers of T2 and T1-hypointense lesions, magnetization transfer ratio, and brain atrophy. In total, 270 participants were randomized to receive monthly intravenous temelimab (6, 12, or 18 mg/kg) or placebo for 24 weeks; at week 24 placebo-treated participants were re-randomized to treatment groups.

    Results: The primary endpoint was not met. At week 48, participants treated with 18 mg/kg temelimab had fewer new T1-hypointense lesions (p = 0.014) and showed consistent, however statistically non-significant, reductions in brain atrophy and magnetization transfer ratio decrease, as compared with the placebo/comparator group. These latter two trends were sustained over 96 weeks. No safety issues emerged.

    Conclusion: Temelimab failed to show an effect on features of acute inflammation but demonstrated preliminary radiological signs of possible anti-neurodegenerative effects. Current data support the development of temelimab for progressive MS.

    Trial registration: CHANGE-MS: ClinicalTrials.gov: NCT02782858, EudraCT: 2015-004059-29; ANGEL-MS: ClinicalTrials.gov: NCT03239860, EudraCT: 2016-004935-18.

    Keywords: MRI; Temelimab; atrophy; clinical trial.

  • I have a question for the neurologists:
    I have never been ‘aware’ of having a relaps – but I have different symptoms that ‘flare’ up when I’m tired, or sick, or hot or cold (colour vision loss, double vision, sensitivity to light, numbness in the upper legs, tingling in the left leg).
    VEPs show that I ‘must’ have had an optic neuritis in both eyes (prior to diagnosis in 2013), and of course there are some lesions in the brain and spinal cord (again prior to diagnosis).
    I just wonder how it’s possible that you’re completely unaware of the ‘main’ attack, but in the years to come, you get or develops symptoms that are all supposed to be a ‘flare’ up? To me it feels like the ‘flare’ is worse than the main event?

  • The 2021 spring UK ms news letter talks a lot of the epstein barr virus at page 36. It seems like they like one of Professor Gavins idea ( and his team ) because they mention the possibility of preventing multiple sclerosis with an EBV vaccine. What are your thoughts on this Mouse Doctor and Professor Gavin ? Do you think research into EBV is becoming more mainstream with the UK ms society ?


  • Shouldn’t there be law against these snake oil sellers?

    Yes I have removed the link so not to drive anybody there

  • They say bipolar disorder is caused by inflammation in the brain and life expectancy for people with bipolar can be lowered by 10 years or more. Do pwBD develop neurological symptoms as they age? If not what’s the difference of an inflammated bipolar brain and MS autoimmune?

  • We know from the OPERA trials that even with RRMS, there’s PIRA (progression independent of disease activity). Patients diagnosed with SPMS and PPMS can still have active lesions and relapses.

    So where is the difference? When does it stop being RRMS and start being progressive MS? How are we differentiating the two?

    • Everything happening in RRMS is also happening in progressive MS and everything happening in progressive MS is also happening in RRMS; it’s just a matter of degree.

        • One way to prove it is to have a vaccine to prevent the epstein-barr virus and show that people that are vaccinated who are at high risk of developing MS don’t go on developing it. Another way of proving it ( in a clinical trial ) is to test an effective antiviral medication against EBV that is also capable of crossing the blood brain barrier and showing that it is very effective in people who already have MS.

          We already have promising antiviral compounds for EBV that could be tested in a clinical trial setting. The speed for which we can show this in a trial will especially depend on how much can we invest together to move this forward and there are some other factors as well. This will dictate the speed for how fast we can prove it.

      • Well, isn’t profG full of it. Make a hypothesis relapses is immune reaction to the “real MS” with no evidence at all, and going around telling patients we have the cause!

        What do you think? I call his hypothesis very misleading. It would be interesting to see you commenting on profG’s work with the same tone to some of other looking-too-hard publications 😉

        Ofc, with enough evidences I will change my views 😉

  • A weekend musing question for Prof G. At what point should a PwMS in their early 60s go, “Hmm, not too sure if my worsening cognitive and memory problems might NOT be MS but might be some form of Alzheimer’s kicking off. I wonder if I should see my doc and get some form of testing done……..?”

  • Glandular fever and long covid, seems some similarities there. Extreme fatigue that can continue for many many months. But will the schools, colleges and univerities begin to recognise both can impact on education children and adults?

  • Case study: Patient on Ocrelizumab. Almost 8 months since last infusion and zero B cells still. Lymphocytes normal and in early 50s. Desire to wait for B cell repopulation for covid vax booster or re-vax. Thought of bridge with Tysabri yet recognize carry-over PML risk since apparently JCV antibody test no longer reliable. Age and lymphocyte count suggest “lower” risk profile for Tysabri vis-a-vis PML.

    Question I have previously posed is why pharma prescribe re-infusion of Ocrelizumab every 6 months where people don’t necessarily repopulate B cells for 5.5 months-3+ years? Wouldn’t better path be to test for B cell repopulation and then if there is, you would infuse again?

    Would Tysabri “bridge” be “over-treatment” where B cells still at zero, and also somewhat increase PML risk?

    Thoughts greatly appreciated.

    • “Question I have previously posed is why pharma prescribe re-infusion of Ocrelizumab every 6 months where people don’t necessarily repopulate B cells for 5.5 months-3+ years? Wouldn’t better path be to test for B cell repopulation and then if there is, you would infuse again?”
      A question MD has been posing for some time and has pondered whether it might in fact be an induction therapy. One answer is of course that Roche makes a lot more money the more infusions that are given and consequently there is little incentive to find out if these may be spaced out much more widely. IMO.

    • MESQ1000 – “JCV antibody test no longer reliable”…… just wondering why the JCV test is considered unreliable? A test is a test, right?

      • My understanding is that if one is on an anti-cd20 such as Ocrelizumab, and desires to switch to Natalizumab, the JCV antibody test will no longer be accurate. Why that is the case is a mystery to me but I did read it somewhere – perhaps on this blog some time ago.

        • Cells from the B cell lineage are the ones responsible for making antibody, which could affect the accuracy of a JCV antibody test as they are depleted by anti-CD20 therapy.

  • Aren’t some B cells regulating/anti inflammatory? If so, couldn’t anti cd20 therapy prove to be damaging to some pwMS, depending on the process at hand in an individual? Certain B cell subsets do promote disease activity, but then other subsets later suppress neuroinflammation?

    I have certainly experienced a decline since Ocrevus initiation almost 1 year ago. I am a female pwMS who is 33, has a low lesion load, only one certain relapse since diagnosis over 5 years ago, which occurred 4 years later, and little/mild evidence of progression over 5 years on annual MRIs, and also in regards to symptoms and clinical evaluation. However Ocrevus has seemed to exacerbate my MS symptoms and sent my fatigue to a new level, without new activity on MRI.

    It seems that most neurologist shrug it off as natural disease progression rather than the possibility that the medication could be amplifying the disease process is a subset of individuals.

    But hey, no lesions enhanced by gadolinium. Therefore it’s “successful” in terms of drug design.

    Targeting B Cells and Plasma Cells in Autoimmune Diseases
    Katharina Hofmann*, Ann-Katrin Clauder and Rudolf Armin Manz


    • Indeed

      Finally, we demonstrate that IFN-β therapy requires immune regulatory B cells by showing that B cell deficient mice do not benefit clinically or histopathologically from IFN-β treatment.


      EAE is a mouse T cell–mediated autoimmune disease of the CNS used to model the human condition MS. The
      contributions of B cells to EAE initiation and progression are unclear. In this study, we have shown that EAE
      disease initiation and progression are differentially influenced by the depletion of B cells from mice with otherwise
      intact immune systems. CD20 antibody–mediated B cell depletion before EAE induction substantially
      exacerbated disease symptoms and increased encephalitogenic T cell influx into the CNS. Increased symptom
      severity resulted from the depletion of a rare IL-10–producing CD1dhiCD5+ regulatory B cell subset (B10 cells),
      since the adoptive transfer of splenic B10 cells before EAE induction normalized EAE in B cell–depleted mice.
      While transfer of regulatory B10 cells was maximally effective during early EAE initiation, they had no obvious
      role during disease progression. Rather, B cell depletion during EAE disease progression dramatically
      suppressed symptoms. Specifically, B cells were required for the generation of CD4+ T cells specific for CNS
      autoantigen and the entry of encephalitogenic T cells into the CNS during disease progression. These results
      demonstrate reciprocal regulatory roles for B cells during EAE immunopathogenesis. The therapeutic effect
      of B cell depletion for the treatment of autoimmunity may therefore depend on the relative contributions and
      the timing of these opposing B cell activities during the course of disease initiation and pathogenesis


      • the effects of the treatments were rubbish and therefore you have to ask about the importance of the biology

  • Hi MD, you mentioned once mRNA vaccines could switch off autoimmunities to certain proteins. How does it work? Thank you!

  • How long does it normally take for a scientific article to be published once it has been submitted to the proper journal ( 6 months, 12 months, 24 months ) ?

    • Usually it can be after revisions it can be around 6 months but if you’re trying to get into one of the big ones and the referees make you jump through multiple hoops, it could be 2 years or more.

      • Thank you mouse doctor 2 for your answer. 🙂 I will keep that in mind for recently funded mouse projects.

  • Nowadays some MS diagnoses are made without relapses, and patients are putting on high efficacy DMTs right away so they don’t get a relapse for many years or ever. What features at diagnoses can help patients/neuros understand how active their MS is?

        • “MRI activity and lesion load are quite hard for patients to see and understand…”

          It’s also hard for Neuros to understand…mri Lesions and relapses aren’t the disease…Brain atrophy is. You can
          understand why patients focus on relapses…because that’s
          the only time many feel any symptoms.

          • I don’t believe in prof G’s theory. I believe relapses are the cause of long-term atrophy, Smouldering has the same pathology as relapses.

          • In response to Anonymous below, and correct me if I’m wrong, I think atrophy is documented frequently in nonactive SPMS, albeit not an easy thing to see, like a spot on an MRI.

  • Biogen signed a deal with InnoCare for Orelabrutinib. I thought Biogen already has a BTKi BIIB091 under development. What could be the incentives to license another one?

    • Biogen are at phase I and they know what the others can do and maybe their version was not good enough. The new acquisition is reported as a CNS penetrant BTKi maybe the Sanofi data which has one of these too

  • I only see one trial for the higher dose ocrevus trial in the rrms which is recruting around 700 participants. Will this be enough to get an approval in the rrms population ?

  • When to refer a pwMS onto a urologist. How does the neurologist know when a female pwMS has groin/bladder pain that it is not due to MS and is due to something else? When to refer them on.

    Does MS cause stinging painful groin pain, that is not caused by a UTI? Has this been seen before in clinic? Thanks.

  • Mouse – if you had just been diagnosed with MS what would be your top 3 treatments to take if you could choose any treatment available?

    Im 30 and have minimal disability but my ms is fairly active

    • You have to make the decisions based on your circumstances and what you are offered depends on your MS.
      For my self I would go for a highly-efficacy, which is an IRT….Why…time is brain. I would practise what I preach.

      • Thank you

        I’ve been offered cladrabine, a choice of 2 anti cd-20 (ocrevus & kesimpta) and tysabri. Or a milder option if I want one, but I’d like the most effective right now.

      • I’m not sure if I’m JC virus’s positive or negative. I’ve not had the test to my knowledge

        • You should assess the status about 55% of people are positive, but this is a risk factor for a brain disease so it is good to know when making choices for example with natalizumab there is an increases risk of this. How often do you want treatments in the hospital at home etc have a look on the MS trust web site

        • The other benefits of cladribine are that it’s probably the safest of your four options, has low monitoring requirements, and won’t inhibit vaccine responses like the anti-CD20 drugs. Tysabri is a good drug, but I still think an IRT like cladribine is better and you can always go on Tysabri later if you have further disease activity. I really think any of the IRTs has the potential to permanently alter disease course and make any future activity much milder than it would have otherwise been.

      • No MD – guess I should have included this point, because I do understand there’s very little a neuro can offer and every PwMS has to find out how best they can manage it. However it would be nice to at least have it acknowledged and perhaps a discussion about how it affects someone/how big a part in their disability it plays.

  • Any guesses on possible connection between RSV and Covid? Houston Texas’s icus are currently alarmingly near full or full for adults with Covid and children’s hospital icus full due to uptick in RSV. Local pediatrician says this is not good because RSV usually peaks in winter, not summer, and it’s unclear why it’s happening now since flu isn’t. Not sure if RSV peaking in other places too. https://www.houstonchronicle.com/news/houston-texas/health/article/Houston-pediatrician-warns-parents-to-take-COVID-16347102.php

  • Nervous Nellie here, how common is RSV infection in adults with MS and will pneumococcal vaccine help prevent an RSV infection from developing into pneumonia? The CDC recently warned of RSV outbreak in US southern states. ☹️☹️☹️ Spread has been seen in Alabama, Florida, Georgia, Kentucky, Mississippi, North Carolina, South Carolina, Tennessee, Arkansas, Louisiana, New Mexico, Oklahoma and Texas. CDC notice https://emergency.cdc.gov/han/2021/han00443.asp. Concerning because no icu beds available here if one were to need it…..

    • I dont know but the good news of the pandemic is that we have a tool to make vaccines to all sorts of viruses

  • Does cladrabine alter DNA and or genes in the long term. I’m wanting kids maybe a year after cladrabine and I don’t want it to effect them. Maybe a silly question but would it make sense to sperm bank just in case or would that not be needed.?

    • Not a silly question, it obviously affects DNA there is some animal data of influencesand when we were doing off label cladribine ProfK offered sperm banking to the males

      • It’s the only thing that worries me about it. I’m going to look into it, cladrabine seams like the treatment for me, just seams like a really great option that I don’t want to turn down. It’s just a major worry for me.

        • search on “cladribine and INN and EMA” or FDA rather than EMA” and then you can see what is known. Its gives a technical summary of the known data including issues with regard to fertility i.e. https://www.ema.europa.eu/en/documents/product-information/mavenclad-epar-product-information_en.pdf. Press “Control)ctrl and the F” key at the same time and then put “fertility” to search the document. You can do the same for any drug you get the summary of product characteristics.

          In mice, there were no effects on fertility or the reproductive function of offspring. However, testicular effects were observed in mice and monkeys (see section 5.3).
          As cladribine interferes with DNA synthesis, adverse effects on human gametogenesis could be expected. Therefore, male patients must take precautions to prevent pregnancy of their partner during cladribine treatment and for at least 6 months after the last dose (see above).

          • Thank you so much for the great information.

            So after the 6 months period, sperm should be back to normal and safe? Would sperm banking only be needed if you want a baby during cladrabine treatment and not after 6 months of a cycle of treatment? So hard to make a decision,

  • What is the shortest research journal paper on the subject of MS? I came across a non MS paper and it was very very short – a diagram and a few words, that’s it.

  • Hi. If bars is right and MS is caused by virus, this implies family can catch MS too. I have young children do I need to be vigilante for MS? Is sonehat symptoms. My oldest is 5 years old. What are the signs I need to look out for. I know I’m being paranoid but it’s better to be fully alert then complacent. I am sure this question is important to alot of people with MS who also have young children. Please answer or tell me I am being silly. I won’t mind either way. Having access to the bedt minds in MS is something no other blog offers. Thankyou in advance. Ps I am on holiday hence the ip is in tenerife. But from London.

    • MS is triggered by a virus and this is thought to be Epstein bar virus which essentially every human catches. In the west this often occurs in adolescence and this is what causes glandular fever.

    • Remember Childhood MS is rarer. Whilst genetics are involved in MS but even if you are an a identical twin then there is a 70% chance the other twin wont get MS so it says genetics aren’t every thing. Children of people with MS are at a small increased risk but your MS genes may be diluted by your partners genes. You can’t do alot about your genes and where you live, but you can ensure that your children have sufficeint vitamin D and don’t smoke and avoid childood obesity and any other risk factors that are avoidable



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