June Q & A 2019


Sometimes you have a question unrelated to the topic of the posts, so post them here.

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  • I am living with SPMS (female in her 50s) and have an asymptomatic UTI. Following NHS instructions to ‘not treat with antibiotics’ means I still have the UTI after a year now. What is this doing to my immune system and the MS? Should I insist on treatment?

    • In our centre, we are a bit more proactive about UTIs and will recommend treatment. Please note we are doing to try and maximise outcomes and to prevent unscheduled hospital admissions.

  • What are the chances that patients on Cladribine will be able to receive additional treatment cycles streching beyond year 4 of therapy? Would the EMA need to approve this change first? If so, by when can one reasonably expect such a change to have happened?

    • Came across the following webpage regarding Cladribine which states: “Following the administration of 2 treatment courses, do not administer additional MAVENCLAD treatment during the next 2 years. Treatment during these 2 years may further increase the risk of malignancy [see WARNINGS AND PRECAUTIONS]. The safety and efficacy of reinitiating MAVENCLAD more than 2 years after completing 2 treatment courses has not been studied”.


      • “…The safety and efficacy of reinitiating MAVENCLAD more than 2 years after completing 2 treatment courses has not been studied”

        Which is why I’m asking my question here. If anyone on planet Earth would have long term knowledge of the safety and efficacy of Mavenclad, then Prof G and the Barts MS Team.

        They might also know, whether patients would need to receive it as “off-label” or whether it would possibly be covered as an approved extension.

        I believe the licensing of Lemtrada also started with two treatments and was then extended later to include a 3rd and 4th dose. Was EMA approval necessary for that?

        • I suspect it is similar to alemtuzumab and people will need to be retreated. Sadl the data is not there. Will the company invest in a trial that will take.years to read out.
          I suspect that the ema will need to agree to extra doses. In reality how.many people.with alemtuzumab do not need.retreatment
          Insuspect a.minority but the data is consirstently.fudged to mask the reality.

          Likewise they continue to hide information on people who stopped responding.

    • It is probably up to the ema, originally the patent life was such that there would.be little.incentive to do such a long and large study.

      We have to expect that many people will need a third course. Most people on alemtuzumab need anotjer treatment at some time.

  • I have been following the research re estriol for years and am interested in trying out hormones but don’t know how to go about doing so. I am 43 y.o. & peri-menopausal, and Dr G’s mention of the following in his last blog post piqued my interest:

    Menopause – if you are menopausal you may want to consider hormone replacement therapy. The evidence on whether HRT makes a difference to MS outcomes is weak but interesting enough to consider it if you are a woman.

    Do I have to wait until I hit menopause? Or are there some options for me? My gynecologist & neurologist are very open-minded. Thank you in advance. JSV

    • I will have a read but they are part T and part B and “the future could bring immunotherapy treatments that can specifically target these DE immune cells, and either eliminate them or stifle their ability to trigger the condition in the first place”….not sure of the basis of the claim, I’ll have to read the paper

      • oK. Can you perhaps write a post on what we know so far about DE cells and what the major pharma group are doing with them? Any trials in the pipeline?

    • More .papers.as this tiny population are seen in other conditions.

      We have been here with the CD20 T cells.

      I.will have a read

  • Hello, I was just diagnosed with RRMS in February & tested positive for the JC virus (.53 titer I think). I’m on Tecfidera & wonder at what point I should get off Tecfidera if the JC Virus level goes up?

  • I understand a phase I human trial will be starting soon for an MS vaccine as described below and would be interested in your thoughts!

    Cyclic MOG35-55 ameliorates clinical and neuropathological features of experimental autoimmune encephalomyelitis. (https://www.ncbi.nlm.nih.gov/portal/utils/pageresolver.fcgi?recordid=5cf583b3dd2142bbe2796cfb)
    Lourbopoulos A, Deraos G, Matsoukas MT, Touloumi O, Giannakopoulou A, Kalbacher H, Grigoriadis N, Apostolopoulos V, Matsoukas J.
    EAE is induced to susceptible mice using linear peptides of myelin proteins of the central nervous system. Specific peptide motifs within the peptide-binding groove of the MHC peptide-complex determines the affinity of the peptide in each animal and the consequent T-cell receptor recognition and activation of the cell. Altered peptide ligand (APL) vaccination is a novel approach based on an effort to induce T-cell tolerance or alter cytokine profile from pro-inflammatory to anti-inflammatory. In the present study we synthesized the MOG35-55 peptide and altered its 3-dimensional conformation to make it a cyclic one (c-MOG35-55). EAE was induced in C57BL/6 mice and pathology was studied on acute and chronic phase of the disease. Our data indicates that c-MOG35-55 peptide alone induces a mild transient acute phase without chronic axonopathy. Administration of the c-MOG35-55 peptide at a 1:1 ratio during disease induction significantly ameliorates clinical disease and underlying pathology, such as demyelination and axonopathy in the acute and chronic phases. Binding and structural studies revealed milder interactions between the c-MOG35-55 and mouse or human MHC class II alleles (H2-IAb and HLA-DR2). Collectively, we provide data supporting for the first time the concept that the cyclic modification of an established encephalitogenic peptide ameliorates the clinical outcomes and underlying pathological processes of EAE. Such a cyclic modification of linear peptides could provide a novel treatment approach for future, patient-selective, immunomodulative treatments of multiple sclerosis.

    • My thoughts….What a load of clap trap. “We provide data supporting for the first time the concept that the cyclic modification of an established encephalitogenic peptide ameliorates”. They have published at least three papers on cyclin myelin peptides from 2014, we did it in the early 1990s after it was reported in Nature…It wasn’t that great and “APL is a novel approach”…who are they deluding, APL was done in the 1990s by Roland Martin and the NIH group and Larry Steinman group and they made MS worse. This airbrushing of history makes me very sad

      • Thank you, I am glad to have the additional information but am sorry this is another example of the airbrushing in your prior post!

        • More .papers.as this tiny population are seen in other conditions.

          We have been here with the CD20 T cells.

          I.will have a read

  • I vaguely remember something being previously said on this blog about Ocrelizumab being ten times stronger or more potent than Rituximab. Is this correct?

    • It is more potent based on the repopulation data repopulation of CD19 takes about 8_12 months with rituximab and 15 months with ocrelizumab

  • Disease rebound after fingolimod discontinuation switching to other DMTs (including cell depleters) is a well known problem. My question is, does this rebound effect also occurs when switching from Fingolimod to Natalizumab ?

    • No reason why not…it is about how quickly the switch agent becomes effective…with natalizumab I think that will however be quick

  • I have a couple of questions about fasting.

    What/who are the controls when examining benefits of fasting? People eating a diet with a lot of sugar and fat?

    What constitutes intermittent fasting? How many hours?

  • I’m loving the garden Prof G 🙂 – I have had a few issues with my MS with regard that it is constant, doesn’t relent & it sometimes takes over my body & I am unable to walk properly or get up from sitting without feeling like I need to arrange for a hoist! My body is going through menopause (I’m on HRT – not sure it is doing much other than my skin looks great) but every month like clockwork, I go through a horrendous bout of mood, physical difficulties. Hormones, I know play a huge part & I wondered if there are any thoughts in researching this more, along with gut & bowel investigations. I feel my MS every day & sometimes we get along, but most of the time – I feel pain, stiffness, heaviness, tiredness, muscle wasting & inflammation whizzing around my skull, arms, and legs. Apart from Pregabalin & steroids – what are the choices – and can we see in the future more research in any of the aforementioned areas?

      • Gawd I’ve enjoyed the laugh out loud moment you’ve just given me MD!
        You also have another fan – in my husband – a fellow lover of IM.

        • Yes! Mum owes me a tenner.

          Having been fairly recently diagnosed I’ve become interested in my future. Are there any statistics/studies available to view on prognosis. In particular, the long term use of dmt and how they may alter the course of the disease.

          • Evidence from the older, less effective DMTs (CRABs) showed some evidence of delaying progression to SPMS in pwRRMS with long-term treatment and starting earlier was better. This is likely to be significantly better with the new highly effective DMTs or HSCT as the long-term data arrives ie the mantra is, hit hard, hit early.

      • Yes! Mum owes me 10 quid.
        Having been fairly recently diagnosed I’ve become interested in the future. I was wondering if there are any statistics/studies available on prognosis? For example, on the long term use of dmt and the impact that can have.

  • Bit late to the party but, what is the barrier to us discovering a cause of MS? I’m not smart enough to think of the reasons why but is it technological, a lack of that type of biological understanding, need more luck? Thanks!

    • Hi Abby
      It’s a great question, as usual the cop out is it’s very complicated and a combination of factors rather than a single cause. It’s also been complicated by the fact that some very eminent scientists and clinicians have sent us down some blind alleys/ vastly over-extrapoloted/interpreted from animal model data and are too eager to hang on to their cherished reputation rather than face facts etc etc. And as you say luck, serendipity, call it what you will, plays a huge part. However, I would say that things are in a far better position in terms of therapies than they were when I started in the field more years than I care to remember, yet we can still do much better.

  • First of all, congratulations for your blog, is so necessary.

    I would like to answer about the LIF NANO of Sue Meltcafe, looks like an incredible clicbait, What is true?

  • YES!!

    Alcohol Consumption Linked to Lower MS Disability

    Multiple sclerosis patients who consumed larger amounts of alcohol had lower rates of disability per the Expanded Disability Status Score (EDSS) and Multiple Sclerosis Severity Score (MSSS), study findings indicate.


    • https://www.neurologyadvisor.com/conference-highlights/aan-2015-coverage/alcohol-consumption-linked-to-lower-ms-disability/?fbclid=IwAR1JqUrDDnkWCOhi_HlZkCQS_-oAoqMX97WM-BY0H3ddYHZ2ndDdqsFJxnc

      Alcohol Consumption Linked to Lower MS Disability

      “the findings are complimentary to several previous but unconfirmed studies that suggest alcohol may be neuroprotective”


      Does your neurologist walk the talk?

      “4. Alcohol – don’t consume too much alcohol, it is neurotoxic even in relatively small amounts.””

      Caneco… em que e que ficamos?


      Ok wait

      No association of tobacco use and disease activity in multiple sclerosis.

      Our results indicate that tobacco use does not directly influence MRI activity or relapse rate in MS. This may implicate that the reported association between smoking and MS disease progression could be mediated through other mechanisms.

      Lets all drink and smoke like there´s no tomorow … 🙂 nothing but party 🙂

      Heavy fuel

      Last time I was sober, man I felt bad
      Worst hangover that I ever had
      It took six hamburgers and scotch all night
      Nicotine for breakfast just to put me right

      My life makes perfect sense
      Lust and food and violence
      Sex and money are my major kicks
      Get me in a fight I like dirty tricks
      Cause if you wanna run cool
      Yes if you wanna run co

      My chick loves a man who’s strong
      The things she’ll do to turn me on
      I love the babes, don’t get me wrong
      Hey, that’s why I wrote this song

      I don’t care if my liver is hanging by a thread 🙂
      Don’t care if my doctor says I ought to be dead
      When my ugly big car won’t climb this hill
      I’ll write a suicide note on a hundred dollar bill
      Cause if you wanna run cool
      If you wanna run cool
      Yes if you wanna run cool, you got to run
      On heavy, heavy fuel
      On heavy, heavy fuel
      ‘Cos if you wanna run cool
      If you wanna run cool
      If you wanna run cool, you got to run
      On heavy, heavy fuel
      Heavy, heavy fuel
      Heavy, heavy fuel

  • MS/Disability/Law questions – there is a question for any expert at the end, please persevere.

    Dear All,

    I am running into issues arguing the point that as the Equality Act 2010 lists MS, along with HIV and Cancer, as a disability.

    P. 5 – point 6 defines a disability as per the legal definition. MS isn’t listed. Subsection 6 of point 6 says: (6)
    Schedule 1 (disability: supplementary provision) has effect. That schedule 1 (p 154) Definition of Disability is what is being referred to. Further on is Schedule 1 p.166 says: Point 6 (1) Cancer, HIV infection and multiple sclerosis are each a disability.

    The argument I am making to anyone who provides any sort of service/concession for so-called disabled people – specifically using the word Disability – is that anyone with MS (the act says from date of diagnosis) is considered to be disabled. Ergo, they ought to be entitled to that concession or service by dint of the fact that they are legally defined as disabled. The lawyers at Oxfordshire County Council seem to think that they may interpret the act as they see fit.

    I do not need a Disabled Bus Pass ( https://www.gov.uk/apply-for-disabled-bus-pass ) at present, but it is my belief that from the Act that a pwMS is considered to be disabled from a legal standpoint and therefore the applicati0n ought to be waved through on that point alone.

    They are clinging to advise on the definition of disability that was spawned by the Disability Discrimination Act 1999a and is in the Transport Act 2000, which the guidance on disability from that is put into the Concessionary Bus fares Act 2007.

    [I know this is very dull, the effect this ambiguity has on less able pwMS pisses me off and drives me to read this stuff]

    There is nothing in the Equality Act 2010 nor the Interpretation Act 1987 that makes me, a layman, think that I have got the wrong end of the stick.

    It was the argument I successfully ran to the Railcard people leading them to add another category of eligibility to their page of criteria. See https://multiple-sclerosis-research.org/2019/05/guest-post-all-aboardfor-your-dprc/

    Question: Am I understanding this correctly?

    Thank you.


  • Immunotherapy Delays Type 1 Diabetes Onset in People at High Risk

    A two-week course of an experimental immunotherapy called teplizumab dramatically reduced type 1 diabetes (T1D) diagnosis rates in people at high risk for the disease, according to newly published phase II clinical trial results. This is the first time a drug has been able to delay or prevent the disease, which affects 2 million people in the United States. Teplizumab is an anti-CD3 monoclonal antibody. The drug interferes with the body’s autoimmune destruction of its insulin-producing cells and can slow the progression of T1D in people with a recent diagnosis.

  • An extra burger meal a day eats the brain away

    “People are eating away at their brain with a really bad fast-food diet and little-to-no exercise,” said Professor Cherbuin from the ANU Centre for Research on Ageing, Health and Wellbeing.

    “The link between type 2 diabetes and the rapid deterioration of brain function is already well established,” Professor Cherbuin said.

    “The damage done is pretty much irreversible once a person reaches midlife, so we urge everyone to eat healthy and get in shape as early as possible—preferably in childhood but certainly by early adulthood.”

    What has become really apparent in our investigation is that advice for people to reduce their risk of brain problems, including their risk of getting dementia, is most commonly given in their 60s or later, when the ‘timely prevention’ horse has already bolted,” he said.

    One of the best chances people have of avoiding preventable brain problems down the track is to eat well and exercise from a young age. The message is simple, but bringing about positive change will be a big challenge. Individuals, parents, medical professionals and governments all have an important role to play.


    Batatas de sofa 🙂

    (couch potatos) be carefull 🙂

  • Just got latest cd 19+/cd 27+ results

    cd 19+ 667 cell/mcL previous result 13/02/2019 442 cell/mcL

    Cd27+ 621 cell/mcL previous result 13/02/2019 18 cell/mcL

    % of (cd19+cd27+) memory B cell in total lymphocytes=1,2% Total lymphocytes

    Lots of memory B cell floating around

    • Been talking with the lab they had change their policy so i guess i was seen 621 memory

      In reality its 20 cell /mcL (1,2% Total lymphocytes)

      I was friking out 🙂


  • Lady and gens

    Prof John W. Prineas

    Multiple Sclerosis: Destruction and Regeneration of
    Astrocytes in Acute Lesions

    There are reports that astrocyte perivascular endfeet are damaged
    in some cases of multiple sclerosis (MS). This study was designed to
    determine the origin and outcome of astrocyte damage in acute, resolving,
    and inactive plaques. Ten acute plaques from 10 early MS
    cases and 14 plaques of differing histological age from 9 subacute
    and chronic cases were examined immunohistochemically. Also examined
    were nonnecrotic early lesions in 3 patients with neuromyelitis
    optica (NMO). Plaques from 3 MS cases were examined
    electron microscopically. The edge zones in each of the 10 acute MS
    lesions revealed a complete loss of astrocyte cell bodies and their
    pericapillary, perineuronal, and perivascular foot processes. Dendrophagocytosis
    of degenerate astrocytes was observed. Astrocyte precursors,
    similar to those that replace destroyed astrocytes in
    nonnecrotic NMO lesions, were present in areas depleted of astrocytes.
    Resolving plaques were repopulated initially by stellate astrocytes
    that stained negatively for the water channel molecule
    aquaporin4 (AQP4). In older lesions, astrocytes were predominantly
    AQP4-positive. Loss and recovery of astrocytes in new MS lesions
    may be as important as myelin loss as a cause of conduction block
    responsible for symptoms in patients with relapsing and remitting
    and secondary progressive MS.

    doi: 10.1093/jnen/nly121

  • Can I be referred to you Prof Gavin Giovanonni by my GP as since having Venoplasty 2012 I have improved. My local Neurologist has changed me from PPMS 20 years ago to now SPMS. I’m looking for some medication to help me finish off my recovery ? So confused by it all. Thank you. x



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