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  • do you think it is appropriate for NICE and the NHS to decide when pwms are sick enough to gain access to more efficacious therapies or should it be down to the neuro and patient to decide ?

    why are pwms expected to accrue more brain damage before being given better treatment ?

    Do you think pwms should be treated before leaving hospital with their first major atack or left for months waiting on more tests ?

    Why are people with neuro degenerative diseases being told certain treatments cost too much ? is there a fair price on health ?

    i know i have asked a few questions but im kind of not expecting an answer as you haven’t answered my questions from november or october

    • 1 No and then yes
      2 . They shouldnt. Some neuris are better than others
      3. Yes maybe ProfK will get a Christmas present and this will become a reality in the trial centres. Imagine on effective treatment whilst the diagnostic work up occurs. Trial is names ATTACK MS. Hopefully Biogen will make this happen.
      4.economics. I have askedProfG why not try PROXIMUS two.

      • Question somehow related to ATTACK-MS. There are a few reports of people on Natalizumab losing their bands. Would it make sense to add an Anti-CD20 at high dose on top of natalizumab to prevent them from returning and then stop treatment or move to first line and control the situation?

        • Yes there are some reports of bands going in some studies, add CD20 on top…Not unless part of a trial so that safety ismonitored

  • Hello,
    I have very active RRMS.
    I’ve been told my next Ocrelizumab infusion is on 22/12 and I have to isolate for at least 2 weeks afterwards.
    I have 3 young children who id have to isolate from. Over Christmas. This doesn’t seem right.
    Could you advise me on different DMTs that might be more suited? I haven’t got an appt with my neurology consultant until October 2021 and my ms nurse is covering 3 hospitals so she’s impossible to pin down. Please help!

    • If you are already on ocrelizumab your B cells are depleted and the next infusion will hang around until the recovering B cells need to be depleted.

      “Ocrelizumab infusion is on 22/12 and I have to isolate for at least 2 weeks afterwards”…Ask what is the logic? Ocrelizumab is present at depleting concentrations for a number of months (its half life is 26 days), it is not like an IRT where the depleted cells come back and even if it was an IRT they would come back that quickly. Maybe if your ocrelizumab depletes neutrophils then there may be some merit iin shielding it is not possible to speak to specific cases.

      Did you have to isolate form your children for earlier infusions..again ask what is now different in the logic.

  • Hi, do you know if there is any research on taking Cladribine post HSCT? (Dr Burt’s protocol) specifically relating to added cancer risk? A little back story…. initially had a fantastic response with improvement in every symptom after HSCT , EDSS went down to a zero but new relapse and symptoms 17 months post, due to start Cladribine in Jan 2021. I do know of one person who did this (Cladribine post HSCT) and did get pretty aggressive BC (first noticed 4 months after finishing Year 1) and almost lost her eye – this one was very fast growing (2 weeks, from size of a white pin prick to 4mm). I know one case isnt causative but it does make me nervous. Thanks, T

  • In this recent post on the secret of teri, prof G stated that patients on anti cd20s are almost relapse free after 6 months. What is the relevance of the 6 month threshold please? do you need to 1st full dose for the treatment to become affective?

  • Is there any disadvantage / safety issue in moving from an anti CD20 medication to an IRT like alem, clad, hsct? for instance, do you need to wait for B-cells to repopulate thereby risking a relapse before killing them again

    • I second this question and add that if you have to wait for a B-cell repopulation and you are a strong responder to the anti CD20 medication, do you wait for over a year with no DMT for the repopulation?

    • Had an in depth discussion about this for HSCT a few months ago. Clear statement: we can start almost any time (perhaps not immediately after infusion to get rid of most MABs first) – B cells get wiped out anyhow.

    • This is just an anecdote, but after a few years on rituximab and multiple relapses, I was put on alemtuzumab. My neuro told me that my lack of CD20s when I started alem might even be protective if they help keep me from developing secondary AI disease, as posts on this blog have speculated. As I had been on rituximab for a few years, who knows when they would repopulate naturally, and alemtuzumab kills those cells anyhow.

  • You organised an amazing conference or training early November this year. One of sessions was entitled something like; ” Should HSCT be a frontline treatment “. I could not attend annoyingly.
    Is there an audio recording I could access? Or will you be running this again?
    Many many thanks for your brilliant work 😎🌈

  • Hi MD – my questions are as follows:

    1. Which Covid-19 vaccine are pwMS able to have? If you’re on treatment, is there a time-line for you & if so, what is it & how is this managed? Also, what is/are the dangers or possible dangers of having the Covid vaccine, if you any of this info, has shown in the studies?
    2. As per other questions, why are the most successful DMDs not given as an option. As mentioned, surely, it would be more advisable to stop disease progression from the outset, rather than expensive healthcare costs for relapses & care as a result of relapses (both mentally and physically – considering mental health seems to be mostly overlooked with the condition) to whom should the decision be given regarding therapies & the discussions the consultants have with the financial bodies, could the patients not be party to this info? As it has a huge bearing on their health & choice!
    3. Why do most pwMS not really go into full details of their symptoms in consultations – TIME, CARE, SUPPORT and too many patients. The latter may be down to where you reside and Country too! Promotion of healthcare tools to support patients should be available, along with guidance on how to use them, would be ideal. A little time invested with the patients, group meeting, regular contact for both mental and physical well-being and changes, are desperately needed, to ensure quality of health & ensure that we are all treated with the same mutual respect of who we are and not just another numbered patient!
    4. Why is there never enough time for consultants/dr’s/nurses to communicate with each other regarding the care of pwMS, if you have other health problems? Is this not what should happen and months shouldn’t go by before you finally get to see someone, when you’re unwell?
    5. Amazing team of healthcare professionals in the UK – along with a fabulous groups of patients too! But can we all try and reinvent the wheel! The quality of care is excellent and I’m grateful for that, but I would like to say that it is like that throughout my journey with my various health issues.
    6. Why isn’t mental health deemed as not important enough for pwMS, yet you can have heart disease and you get to see a psychologist? If a pwMS has to suffer pain every-day (and I do) – why isn’t that not looked upon as urgent mental health support. If you have a strong mind – you can train yourself with techniques, CBT, distraction and busy exercise routines, all help. But if you aren’t equipped with this disposition – those pain days can get you so down.

    I have lots more – but I’m guessing from my fingers (arthritis, yep, another blimming pain layer 🙁 – become sore! I hope it’s not too many and you can answer at least some of them.

    Thank you and I hope you are all keeping well and safe from the dreaded virus.


    • 1aWhich Covid-19 vaccine are pwMS able to have?
      Looks like all that are likely to appear.
      1bDangers of vaccines
      Injection site reactions
      2 yes
      3 time constraints I gues
      4 time constrainsts
      5 no response needed
      6. good point

  • Covid-19 patients who received cancer treatments that suppress their immune system may remain contagious and able to spread the coronavirus for two months or more, according to a study published on Tuesday.

    The US Centers for Disease Control and Prevention (CDC) currently recommends that when patients have compromised immune systems, healthcare workers follow extra precautions such as wearing respirators instead of face masks and isolate patients for up to 20 days after symptoms appear.

    In the new study, researchers analysed sputum and swab samples from 20 immunosuppressed cancer patients infected with the coronavirus. They found three were contagious for more than three weeks after their symptoms began, including one who remained contagious for 61 days.

    The three patients had received either a stem-cell transplant or therapy with genetically engineered immune cells called CAR T-cells within the previous six months. Two of the three had developed severe Covid-19. None of them had antibodies to the virus.

    (Taken from report in The Guardian today)

    As DMTs result in being immunosuppressed it seems sensible to take this on board, both for the NHS and for PwMS – do you agree?

  • Any advice on what a patient should be seeking to be included post IRT (hsct) in terms of their care so as to monitor /suppress disease going forward? Obviously mri and symptoms need monitored, but previous posts on this blog make we wonder if lumber puncture should be included to monitor nfl, and if maintenance dmt such as aubagio should be considered or an antiviral would be recommended … a check list world be helpful 😫

    • There is no evidence so if we suggest anything it is just personal bias. No evidence that ani viral are of value

  • Hello, and Happy Holidays!

    Could you please tell me which part of nerve cells’ communication MS affects most… the electrical parts, or the chemical parts?

    Also a second question if you have time. As nerve fibres begin to die from demyelination, can they grow back if remyelinated? This is speaking to the news of remyelination therapies getting closer to being available someday.

      • How long does it take a nerve to die? For instance, new lesions can make nerves prone to die off but at what point in time following a relapse can a patient take some comfort that this is not going to happen? Is there any rule of thumb

        • Great questions 🙂

          I think it depend on the quality of the damage (lesions)

          ü Persistent inflammation at the lesion edge is not only a major barrier for remyelination, but can exert ongoing damage to the
          surrounding tissue.
          ü Long-term lesion evolution (dichotomy):
          • rim+ lesions tend to remain stable or expand over time;
          • rim- lesions tend to shrink over time11
          ü Rim+ lesions = more likely to be destructive (higher 7T T1 values) -> in line with impaired early lesion repair8

          Longitudinal MRI History of Lesion Repair Based on the Presence or Absence of a 7T Paramagnetic Rim


          In vivo characterization of cortical lesion demyelination and remyelination in early multiple sclerosis by quantitative 7 Tesla MRI

          Cumulative CL number was 54. At follow-up further CL demyelination was found in 5/7 patients within 17/54 CL (17% of total CL), remyelination was found only in one subject within 2/54 lesions (2% of total CL), 35/54 stable CL (65%) were found among all subjects. Demyelination status at baseline was a predictor of further CL demyelination at follow-up (p< 0.01)


          Iron rim lesions in Multiple Sclerosis at 7 Tesla Magnetic Resonance Imaging: a 7 year prospective longitudinal study
          Diffusivity data suggests progressive lesion-independent demyelination in NAWM of MS patients: a 5 year study


          Shrinking MS lesions – anything to take note of?


          So has you can see its very heterogeneous

          But please try to take some conclusions (if possible)


  • Goosebumps on face – evenly distributed all over and even small size, lasted 2 weeks.

    Is it a sign of relapse and what should the patient do?

  • AI just made the biggest breakthrough in biology. Clock is ticking. MS breakthrough is also round the corner. Pharma day of reckoning is coming …. soon the names will become AI1, AI2, PROF AIG, PROF AIK.

    • I recall someone on the forum that works in AI stating that it was coming to our rescue a few months back. Their words were ‘how do I know….I work in AI’ it must have stuck with me. Perhaps they can give some insight as to what this may mean for MS patients in the (hopefully not too distant) future

      • There are different types of AI models. The one used to solve decades old biology problem of the shape of protein molecules i suspect uses unsupervised model. Which basically means you feed it all the information and using powerful mathematical models it find relationships scanning all the information it is fed. However some these findings may be just coincidental so still will require scientifically trained individual to deciper the real discoveries from those just coincident. Doesn’t really cost so much to setup. Just needs to be fed all the information in any format. The problem we have its not that MS won’t benefit hugely from this technology. Just people stuck in their old ways and scared of losing their jobs. But the genie is out of the bottle. The discovery made by deep mind will send a shiver down the spines of all those researchers who thought the gravy train will never stop.

        • Perhaps Deep Mind will also find the remedy for hubris in addition to everything else its going to solve. ;-).
          Can someone please point out this gravy train as it doesn’t seem to stop at our station.?

        • Also, AI (Artificial Intellegence) does not exist yet (if it ever will or indeed if it ever should). What we are talking about here is machine learning utilising vast amounts of computing power.

          • Thanks MD2. I must apologise for some of my of the cuff remarks as their really not written with barts team in mind. But talking generally about the researchers working for pharma. I guess when I write on this forum is to blow off steam, When really the aim of the forum is to exchange ideas and promote MS understanding both among patients and researchers. A noble effort. Nevertheless no one should be above critical analysis. Like absolute power, absolute goodness corrupts. As for you AI comments,. The brain is also a large mathematical computer, albeit a quantum one. The point of singularity (Machine intelligence equals Human intelligence ) is at best 5 years away. Then its game over for humans. In the long term what becomes smarter than you will never be shackled. They will out think you and break their shackles. Watch my words.

  • 😄 Happy holidays to all of you!!
    I was diagnosed in 2002 and treated with Avonex. I gave birth to my son in 2006-good pregnancy & labour. Then I was treated with Tysabri, until 2010, when I stopped it, because I started to feel unstable. I am now expecting Siponimod to free me from my wheelchair & isolation…

      • Sure if you want. Its what I do for a living. Err I pretend to do for a living. My real job is trying to read the entire Internet.

        Let explain the problem so you may appreciate the tsunami thats about to hit research in any science. Here is the problem solved by Google deep mind as explained in 1969 by Levinthal

        Proteins are macromolecules which possess several unique properties. They are very large (containing 2,000 or more atoms) and complex. Their structures show no obvious regularity but a very subtle regularity is apparent upon close examination. We know from the fact that proteins may be crystallized and further from x-ray crystallography that each atom occupies a unique place in the relative 3-dimensional space of the molecule. If we consider a protein containing 2,000 atoms with no structural restrictions, such a macromolecule would possess 6,000 degrees of freedom. We know, however, from x-ray studies and other techniques as well, that there are indeed certain structural restrictions in a polypeptide structure. For example, if we schematically indicate a polypeptide chain as in Figure 1, we find that the 6 atoms in each unit indicated by the dotted lines lie in a common plane. Considerations of such factors allow us to predict only 450 degrees of freedom in a protein structure containing 150 amino acids, for example. Of these 450 degrees of freedom, 300 would be due to rotations and 150 would be due to relative bond angles of the side chains.

        There was earlier (1960s work) attempting to predict the 3-dimensional structure of some polypeptides from primary sequence information.

        If we begin with a set of bond angles and bond lengths and go to 3-dimensional coordinates (via vector matrix multiplications), we can build a 3-dimensional image and display it on a computer controlled oscilloscope. If we know the coordinates of any two atoms and their interaction energy functions, could we extend this treatment to sum the total energy of a given polypeptide or protein structure?

        How accurately must we know the bond angles to be able to estimate these energies? Even if we knew these angles to better than a tenth of a radian, there would be 10^300 possible configurations in our theoretical protein. In nature, proteins apparently do not sample all of these possible configurations since they fold in a few seconds, and even postulating a minimum time for going from one conformation to another, the proteins would have time to try on the order of 108 different conformations at most before reaching their final state. We feel that protein folding is speeded and guided by the rapid formation of local interactions which then determine the further folding of the peptide. This suggests local amino acid sequences which form stable interactions and serve as nucleation points in the folding process.

  • I wondered whether if the AZ vaccine will be contraindicated for those of us on cd20 treatments or with MS generally (maybe due to adverse events) this has been fed into the prioritisation for vaccine roll out? I can see how we wouldn’t be first in the queue ahead of older people, but knowing there might be some of the other versions left over would be good!

  • Can you say a little about the differences between the different types of stem cell therapy, please? It looks like HSCT has gotten the most attention; what’s the current state of knowledge on things like MSC, NSC, and iPSC?

    (And thank you for this blog. It’s the most informative I know of.)

  • There have been several discussions on the microglia being good or bad and a clear answer to this is not yet available. BTKis are claimed to inhibit microglia activity. There are several trial ongoing and many phase 2 were concluded without highlighting any worsening that would raise a red flag (I am thinking of Something like the atacicept story). Should we think that they may be actually doing something good beyond suppressing relapses or just no harm?

  • It’s almost Covid-19 vaccine time!
    My trust is preparing to be up and running at the beginning of next week to administer to frontline staff. This is great news but I’m due my first full dose of Ocrevus in 2 weeks. Am I right in thinking the timing isn’t ideal? Oh well……

      • Looks like It’ll be soon for me according to the work email I read today. As I’m due Ocrevus in 2 weeks is it even worth me trying to get it ASAP?

        • If you can be vaccinated before ocrelizumab it has the best chance of working the covid 19 pfizer need three weeks to complete and proably 4 weeks to be optimum. So this needs to bbe balanced with the need to control your MS. Speack to your HCP

  • OB bands – I came across an article making a statement that Asian MS population has a lower percentage of patients with positive OB bands, some studies suggest below 50%. And the OB bands comes and goes without DMT treatment – the majority of people in the studies were only treated with corticosteroids at qualified relapses.

    Gene differences of different ethnic groups? Is the appearance of OB bands linked to disease course?

  • Short copy paste from previous ProfG post.

    Months ago ProfG wrote about an epiphany he had about first patients being treated with alemtuzumab and free from disease for more than 10 years.
    I was wondering: did anybody test those patients to check their immune system population characteristics in periphery and CSF?

    • “did anybody test those patients to check their immune system population characteristics in periphery and CSF?”

      Yes..early b cells skew to immature state and slow recovery of memory b cells.
      Perhaps Mark S. Freedman known to pop up on this board at times…will show up and possibly update/elaborate on this…one can always hope..

      “Early T-cell recovery is characterized by an increase in the proportion of memory T cells with a regulatory phenotype, followed by a gradual return of CD8+ and CD4+ T cells. Although the regulatory function of Tregs following alemtuzumab treatment has not been formally evaluated in MS patients, their enrichment in the recovering CD4+ pool may contribute to the persistent control of inflammatory processes in MS. Changes in the proportions of Th2/ Th17/Th1 subsets and the cytokines that they produce may also act to “reshape” the immune response post alemtuzumab treatment.”

      p.s. hsct is better…


  • I have been trawling through the archives on the blog regarding alemtuzumab. The overwhelming view is that to be effective / a potential cure, this treatment needs to be given early in the disease course, before MS has ‘set up shop’. However, when pushed on a definition of early, the responses are vague ‘earlier the better etc’. I know it is not easily defined. However, are you able to offer a little more guidance? lesion load, EDSS, 2 years post diagnosis etc? I ask because patients are using the information on this blog to push their neorologists for certain treatments. As a case in point, a patient relapsing on Ocrevus could in theory push for treatment with Alemtuzumab. However if already too late to the table, they may only end up with a secondary autoimmune issue on top of continued relapses (since the date for Ocrevus turning off relapses is just about the best). This may be Prof G’s area, if he is well enough. I get the impression that a lot of CD20 patients are wondering the same so it is an important topic in my view

    • I would be that patient on ocrevus pushing alemtuzumab even if not relapsing and given that I could be treated with anti cd20 to prevent secondary autoimmunity. There is the whack a mole paper that seems quite good. Unfortunately, this and many other combination treatments cannot be given outside a trial and setting one up seems to be a nightmare. This is connected to one of my posts above about testing people after alemtuzumab been well for more than 10 years. This could help to define when to use alemtuzumab.
      Also people push on alemtuzumab because they are aware of what they are risking in the long term and they prefer to front load the risks of using a big gun early. Finally, there is a gap between what patients are willing to risk and what neuros think it’s appropriate to risk and this in the best interest of patient health of course. And this can occur in both directions.

      • Sounds familiar, except for me it’s HSCT rather than alemtuzumab.

        I’m told I need definite radiological changes but the radiologist says my MRI are on the rather blurrsy side to begin with. So go figure.

        Maybe I should ask about alemtuzumab next time round…

    • “treatment needs to be given early in the disease course, before MS has ‘set up shop’. However, when pushed on a definition of early, the responses are vague ‘earlier the better etc’. I know it is not easily defined. However, are you able to offer a little more guidance?”

      Apparently..not as your question has been repeatedly ignored. Anyone still solidly in rrms could give Alemtuzumab a shot…edss 2..3..4.. is heading to early spms but if it works it could knock it down lower…and if it didn’t you could always do hsct after..yes it’s been done. Or just do hsct first as it’s been shown superior to alemtuzumab.


  • Are PWMS more likely to develop secondary autoimmune diseases, even if they are not taking DMTs such as Lemtrada?

  • Alemtuzumab treatment 9 & 10 years ago. ITP 2 years ago, haematologist thought flu vaccine had caused it rather than alemtuzumab. Neurologist thought possibly either.
    Spent yesterday in A&E after bruising, platelets down to 36, ITP again but not had flu vaccine this year. Seeing haematologist next week in outpatients. Any thoughts? Otherwise well.

    • Just rereading earlier questions regarding alemtuzumab. I received alemtuzumab as first line therapy on first ms attack, though it was a whopper, paralyzed from chest down.
      At that point I barely knew what MS was, let alone about treatments. Thankfully I was treated by a very forward thinking neurologist who prescribed it prior to licensing with the intention of hitting the MS back as hard as it had hit me.
      Once home I began researching & to be honest, I was shocked at the nature / strength of the alemtuzumab. Almost 10 years later to the day, I have only experienced one very mild relapse 4 years ago. Apart from that, I am fit and well, still working & only have some mild leg weakness, a residual from first attack.
      Whether this ITP proves to be a side effect of alemtuzumab remains to be seen… but I do feel extremely grateful to that original neuro who treated me for literally giving me my life back.

    • Thank you for your interesting story, I trust the haematologists will sor you out, but if it is alemtuzumab it is a long time after dosing

    • Treatment

      With rare exceptions, there is usually no need to treat based on platelet counts. Many older recommendations suggested a certain platelet count threshold (usually somewhere below 20.0/µl) as an indication for hospitalization or treatment. Current guidelines recommend treatment only in cases of significant bleeding. Treatment recommendations sometimes differ for adult and pediatric ITP.[15]


  • If they can produce an anti-coved vaccine so quickly and efficiently, what’s the hope of an anti- EBV? Or is it more complicated or political than that?

  • Mouse doctor….or Prof G, what are your thoughts on AMM01 for blocking EBV? If EBV reactivation is driving disease progression could it be stopped if AMM01 can block it? Or is this just wishful thinking? Also is there any update on the trail from Atara bio?

    • Atarbio…press reports…but soory I dont do these are this is free advertising
      AMM01 interesting not sure antibodies are the way to go but simple enough to test..use it in mononucleosis

    • Yes and no. Only those in the CNS. Taking out all plasma cells and plasmablast is the equivalent of a missile with a nuclear war head.

      • That’s true but would likely be a total reset. Following MD post on CAR-T I thought that during the Ig suppression time frame one could treat with Ig from donors to allow for a safer recovery, something like the treatment is given to people with x-linked agammaglobulinemia. Expensive but not forever. The antibody for sure will be less effective than a small molecule so it may be better to wait for the first round of results (and to watch this space 🙂 )

    • I have to say NSS.
      The original question is guff…we dont know why oligodendrocytes dont fully remyelinate…to some extent yes we do…The authors need to do some reading. But they asks is it intrinsic to the oligodendrocytes that they dont repair…but the fact that the myelinate in the first place says this is not the case next there are numerous studies show switch factors that allow myelination/remyelination…so you make oligodendrocytes from some one with MS and ask can they myelinate…of course they will and guess what this is what this study shows. It says you can make oligodendrocytes from any body

      Remyelination failure in multiple sclerosis (MS) is associated with a migration/differentiation block of oligodendroglia. The reason for this block is highly debated. It could result from disease-related extrinsic or intrinsic regulators in oligodendroglial biology. To avoid confounding immune-mediated extrinsic effect, we used an immune-deficient mouse model to compare induced pluripotent stem cell–derived oligodendroglia from MS and healthy donors following engraftment in the developing CNS. We show that the MS-progeny behaves and differentiates into oligodendrocytes to the same extent as controls. They generate equal amounts of myelin, with bona fide nodes of Ranvier, and promote equal restoration of their host slow conduction. MS-progeny expressed oligodendrocyte- and astrocyte-specific connexins and established functional connections with donor and host glia. Thus, MS oligodendroglia, regardless of major immune manipulators, are intrinsically capable of myelination and making functional axo-glia/glia-glia connections, reinforcing the view that the MS oligodendrocyte differentiation block is not from major intrinsic oligodendroglial deficits.

  • BBC Newsroom Southeast this evening did a piece on MS.
    It focussed on the MS Society having highlighted that 1 in 5 diagnosed are under the age of 30.

    Im assuming I correct in my angry reaction to the sound bite interview with a member of the MS Society staff who said that by 2025 they’re hoping to be able to prevent MS from progressing (‘getting any worse’ I think are the words that were used)

    She made it sound as if in a mere five years time MS will be a disease that can be completely suppressed and controlled. No doubt I’m going to be one of many being asked if there’s nothing any longer to be worried about😠

    • They are heading for a fall…we have seen this over and over again and are soundbites for a funding call…they may do some trials. A definative trial will take 4-5 years.

    • You’re right Fi, statements like this are mere guff, with no basis in fact and you get it from every charity.

      • Honestly MD and MD2 it’s So wrong to put out this sort of statement on national TV – the young woman in the piece is 29, using a wheelchair and only recently diagnosed. I wanted to contact the BBC and ask they provide her with the Blog details!

    • David. Wraith and others used inhaled peptide for tolerance induction about 35 years ago, we showed you can use antigen particles to tolerise, The Chicago crew showed you can use nanoparticles…So whats really that new.

    • Ok, nanoparticles old news, what about inhaled albuterol??? I know There is an observed significant inverse relationship between pwMS population and people diagnosed with asthma who are treated with Albuterol and/or inhaled steroids. I believe it’s speculated that albuterol up-regulates beneficial T cells. At least one study found that it was a good add on to copaxone, and improved results. I had followed this idea closely while I was on copaxone, and I am aware of some pwMS who sought out off label use of albuterol for this purpose https://pubmed.ncbi.nlm.nih.gov/20837847/. But I don’t know current data on this view albuterol is beneficial to pwMS. Are inhalers as an add on something that piques mouse doctor’s interest?

    • No point in commenting until the trials are done. Again the effects are not miraculous and so stem cells are not the complete answer

  • Hi All

    The resident anonymous AI champion here. After months of moaning and complaining I have decided to get off my fat butt and start using my BI (Business Intelligence) / ML (Machine Learning) skills for the advancement of medicine, To start off, I have picked a topic that I know has been done already that is building models to automate diagnosis of MS from MRI based data by identifying T1 and T2 flairs. This will pan out into a more advanced model at latter stages as I pick up the experience. My question is as follows, in order to make the model predict accurately it needs large amount of normal and abnormal MRI’s. Is there a resource where I can download this data for free? Please do not dissuade me or say its pointless or say it will never amount to much. Just a pointer where I can get anonymous MRI data. Do not need to know patient names, Just abnormal suspect MS. Normal MRI. Thanks

      • Maybe so, but its purely a academic exercise to serve two purposes. 1) Give me something to show when applying to pharma. 2) Give me the insights and challenges involved in applying ML to the medical field. As for domain expertise. No direct experience of MRI, but was a biochemical engineer. Let’s see what happens. Not a data scientist but hard core Data Engineer. So more hands on.

  • I was curious about any association between cataplexy and MS. For a couple of years before my MS diagnosis, I had noticed that whenever I was standing and something made me laugh, I felt weak in the knees, as if I was about to collapse (it only lasted for a split second though and I never actually went down). I never knew there was a name for it until I came across it recently while reading an article about narcolepsy (which I don’t have). I mentioned it to my neurologist and she was skeptical… which she is about everything I tell her. I still experience it but so far it hasn’t become a big issue… so far. Anyway, just wanted to throw it out there!

  • Klaus has just shared a tweet from Dr Barry singer which has a link to a document for the Pfizer vaccination which implies or actually says that people with a history past or present of autoimmune medication should not use the Pfizer vaccination is this correct?
    Sorry I cannot attach the link

    • you have mis interpreted it in the trial protocol people on active immunotherapy were excluded for the trial it does not means they should not take it

      • Sorry about that but thank you for replying.
        I am now really confused because my neurologist is now saying that the Oxford vaccine should definitely be avoided because it is live
        You also said this at one point but I have since read that the Oxford vaccine is ok because it is not a traditionally live vaccine so is ok whether you’re on a DMT or not
        My neurologist is not offering any advice officially which I can use when talking to my GP
        What is the definitive advice as to which vaccine is ok and effective to use if you have MS yes regardless of whether you’re on treatment or not?

        • The Oxford vaccine is not “live” as it is has been modified so it is incapable of replicating itself once in cells. This is unlike other vaccines such as MMR which use weakened forms of virus which will not cause disease in normal subjects but not recommended for those with weakened immune systems.

  • Many people with MS seem to obtain benefit from medicinal cannabis. I recently discovered that CBD can prevent some chemotheraputic agents, like rituximab, from working in cancer. Can you comment on the implications of this in MS treatment please.

    • You need to provide a link to your source. Interfering with the action of rituximab seems rather unlikely to me though it has been reported that concomitant use of cannabidiol oil with steroids, naproxen, tramadol and amitriptyline can potentiate adverse events.

  • I was thinking about the de risking of Anti-CD20 because of decreased antibodies production and I thought “what is happening to people taking CD19 car t like kymriah?” This treatment, to my understanding, should suppress B-cells forever so aren’t those people going to be deprived of antibodies in the long term? It should be seen much earlier than Anti-CD20

    • I dont know, for definate, but the we have the data for 18 months after 3 courses (this would be the samae as alemtuzumab and cladribine so does for 12-13months. We need a proper tiral

  • First of all i want to thank everybody who is working/worked on the Blog or si sharing usefull content on it. As a person with MS who wants to find out more about the disease i find it very helpful. My question is about NFL and what it is worth from a patients perspective. So i am a 37 year old male who got diagnosed with PPMS 379 days ago and who is on Ocrelizumab since march this year. I am at the UMC in amsterdam where they measure NFL in serum. Since covid they have a protocol for orcrelizumab where they track B cell count and only give a next dose when your count is above 10000/ml. They draw my blood ervery month and i have the following 4 NFL values: 6,8/6,0/4,9/4,4 pg/ml.

    Can you give me your take on the following 2 questions:

    1: Can i still have more loss of axons and neurons than a healthy person with a NFL as low as 4,4?

    2: Is it strange that while B cell are rising my NFL is lowering?

    Thanks in advance

  • I’ve just had a close relative phone me about the BBC website article about Advance MS and the Statins trial by Caroline Wyatt.

    My close relative knows I have RRMS but she thought it is the same as Advance MS. I know there are some that argue that there is only one type of MS but in my case this is not helping me.

    It gives the wrong impression, as my MS is invisible. I find it pretty frustrating.

  • If a patient’s MS continues to worsen following the two treatment cycles of Mavenclad, would it be permitted or recommended after four years to try a course of Alemtuzumab to try and slow down the increasing disability – or considered too late or too risky?

    • Maybe ProfK, but the question one must ask and that is, Is the worsening due to active lesions and relapses or the slow-burn?. If the former is happening cladribine is not working effectively and one should be asking about another course or a switch (pS Im not a neuro), if it is the latter will alemtuzumab do any better

    • Luis, I’ve suspected that acute MS attacks can be preceded by simple focal seizures, based on my own exerpience. Hours before my severe attack a finger on my right hand was twitching/ contacting in dramatic way. My lesion was on left side. Other MSers have shared similar experiences with me. I think such seizures are underreported. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3743331/
      the neuro is occupied with how your strength, motor skills, vision, and speech are affected and reporting that your finger or face twitches is of lesser concern or considered unremarkable. I take the sensations as a warning my MS is gearing up. Query, Would EEGs be early warning of MS activity?

  • After 6 years of DMF, and as many years NEDA, my neurologist and I decided to go off DMF, at least for a while (given the quite serious side-effects). I’ve been off for a few months now, and I feel no different, except for the welcome absence of GI issues, flushes, rash, hair loss, infections,… Given how DMF works (reduction of memory cells, CD8+ and CD4 T cells) and the enhancement of CD4+ and CD8+T cells and memory cells the covid19 vaccine aims for, I’m reluctant to rush into the covid vaccine. If I still was taking DMF, I think I could indeed get the vaccine (even if it would be possibly less effective). However, having just quit DMF, I’m not sure I want to ‘rock the boat’ just now. Any thoughts on that would be greatly appreciated!

  • Whising all barts blog team a happy christmas ,especially Prof G hopping is recovering well a,stay strong

    Luis Frernando

  • Last day of the year in detective mode

    Published data from Moderna COVID-19 vaccine trial show 94.1 percent efficacy


    Efficacy and Safety of the mRNA-1273
    SARS-CoV-2 Vaccine


    Peer review study bla.bla,bla

    Then you dig down where the money flow and you found out that the head of the study

    Dr. Baden is a Deputy
    Editor at the New England Journal of Medicine.

    Dr. Baden is involved with,moderna

    Another author

    Hamilton Bennett

    Ms. Bennett
    reports personal fees from Moderna, Inc, outside the submitted work;

    Employee of Moderna, Inc. and hold
    stock and stock options


    Dr. Deng

    Employee of Moderna Inc.


    Dr. Graham

    reports In addition, Dr. Graham has a patent Patent Application No. WO/2018/081318
    Prefusion Coronavirus Spike Proteins and Their Use pending, and a patent US Patent Application No. 62/972,886
    2019-nCoV Vaccine pending


    Dr Shu han

    Employee of Moderna Inc. and hold
    stock and stock options


    Dr. Ivarsson

    reports personal fees and other from Moderna, outside the submitted work


    Dr. Knightly

    Employee of Moderna and hold stock
    and stock options

    Dr. Leav

    Brett Leav is an employee of
    Moderna Inc.


    Dr. Miller

    is an employee of
    Moderna Inc.


    Dr. Pajon

    I am an Employee of Moderna Inc.
    and I own stocks in the Company


    Dr Zsks

    is an employee of
    Moderna Inc.


    Dr Zhou

    i am an employee of Moderna TX


    So my question who can you trust?

    Almost half of the authors of the study are modena employe and have stock option … bla bla bla

    Ask yourself who can you trust

    Happy new year

    Luis fernando

    Remind me of a nice song by Qotsa


    • There is no evidence that you shouldnt take these agents….Just go a great idea lets dump the name the oxford or Astrazeneca vaccine label and call it Covishield

By MouseDoctor2



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