Ask a Question July


If you have a question unrelated to other posts.

This is the place for you

 Pic by MD2 Derwent Water

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  • I'm a layperson so what I'm asking might not make biological sense. It's probably not a simple question either. Wish I'd paid more attention in school!

    I sort of understand that T-Cells manage to traverse the blood brain barrier and they attack myelin. Do all T-Cells do this or do only a few go rogue?

    I've wondered if, when the BBR repairs itself, are the the T-Cells moving around in a place they shouldn't be causing havoc, leading to inflammation and degeneration of myelin. They die off and then you're OK for a while until the BBR lets more in, then the process starts over but given the pre-existing degeneration, the effects are incrementally worse.

    Or is it once they are in, they are in and they will just cause havoc for as long as they can?

    I guess my question is, for RRMS probably, is it an opening/closing of the BBR "gate" that gives rise to relapses and remission, or is it more random than that?

    Thanks! P.S. Loved the photo.

  • Did MD1 and ProfG desert this blog for good?

    They have probably posted no more than a handful of good posts between then since the beginning of the year.

    Is this the beginning of the end of this blog as we knew it? Would we need to see the emergence of another Zamboni to brig it back to life?

    • I am still here, but my phone have been locked out of the comments for a couple of months and is not allowing me to comment.

      The blog bosses have been aiming for one post a day and there are more people posting. Likewise we can only post on the same thing so many times.

      I have also had a lot less spare time for the past few months, for a number of reasons and so simply not had time to post.

    • MD you are missed from the blog! We are looking forward to get your phone fixed 😛

      Wish MD2 was more active too :/

    • I’m more confused than ever. Is the consensus, that with non active MRi scans , age in the 50’s, and progressive MS , there is no effective treatment to preserve upper limb function? I Know Ocrevus only nominally slows progression, less than 30%. I’ve
      been reading about saving hand function, but it seems the above mentioned subset of MS may be left out in the cold.

    • Try this 🙂

      "Graham Walker"
      I can concur from my own experience : I was a road cyclist, competitive , in my younger days and now , ppMS, 5 years into diagnosis, I ride on the road 25 miles (40 km ) 5 times per week , weather permitting. My Neurologist and other professionals say they are amazed at how I'm holding progression.
      I am able to do this because I'm mentally adapted because of my past experience, I utalize clip on pedals and shoes, and I have a very supportive wife and family.
      Exercise is undoubtedly very important !

    • Maria..yes you are correct..really is no treatment/cure
      for progressive ms. But this was the first trial to actually
      reduce EDSS in a 60 y/o ppms and spms patient. So there is
      hope for people to stop progression and improve going forward.

  • MS Society asks for our opinion to test existing drugs for MS:

    What existing medicine do you think could help in MS?

    Please join our initiative! Our consortium want to hear from everybody, especially people living with MS. If you can suggest a drug that that may have the potential to slow progression please email by 30 July 2018.

    It needs to be a treatment that’s already licensed for another condition, and we’d like as much information about it as you can give. The consortium will analyse available information on each drug to identify the most promising. We expect these to be the first drugs tested when the platform is ready.

  • If it is thought that B and or T cells are part of the problem in MS why can't we analyze some of these in pWMS and see what kind of receptors they have to pinpoint the kind of antigen that is leading to the inflammation and better understand the pathology ? Or at least develop a biomarker based test ?

    • The "antigen" for T cells has been looked for for decades but nothing convincing has ever been found. Same goes for the antibodies produced by B cells in the CNS ie this isn't autoimmunity as such in the classical sense more an aberrant immune response in the CNS the triggers for which are still frustratingly to be understood.

  • What is the (updated) data on the likelihood of progressing to Secondary progressive MS factoring in being on a DMT? (The data I've seen so far is that generally 80% of people with RRMS 15 to 20 years after being diagnosed with RRMS will progress to SPMS.

    • I think the doctors on here (and knowledgable MS doctors generally) believe that MS is one disease, not three. Whichever kind a person has, there will be 'progression', in the sense that they will have lasting scarring on their brains (with the possible exception of people who have Lemtrada or HSCT early on in their disease). Whether the scarring manifests as permanent disability depends where it is and how bad it is. This in turn will depend, in part, on the treatment they have had on the way. So there are no general stats on this – if someone has been put on an effective DMT and changed to another if the previous one becomes ineffective, they are much less likely to end up with permanent loss of function (is that your definition of SPMS?).

    • Thanks a lot for your explanation! Truly appreciate it. I have RRMS diagnosed in 2014 and I'm 34 years old. I'm on Tysabri and feel good ad am stable. Admittedly, I do however think about the future & wonder whether HSCT or Lemtrada is worth switching to

    • Tysabri is a very good drug, but if you have JC virus then there the risk of PML and so switching may be reckomended, If not its a very good drug.
      COi None

  • Good morning and congratulations for the blog.

    If as the MS is believed to be caused by a virus and has more incidence in high latitudes, is it possible that the hours of sun influence the number of viruses and not the MS? Like malaria.

    Thank you.

  • Concerning the search for what went wrong with Daclizumab, I understood that the Neuropathology Department in Göttingen (where some of the Zinbryta patients had died) issued a statement indicating that the suppression of the Il-2 receptors had apparently led for some to an increase in eosinophils which in turn resulted in cases of eosinophilic meningitis.

    Any comments?

    • Germany recently informed the European Medicines Agency (EMA) that seven patients with multiple sclerosis (MS) had developed immune-mediated inflammation of the brain (encephalitis) during treatment with daclizumab beta (Zinbryta). Three of these patients also had a severe allergic reaction (drug reaction with eosinophilia and systemic symptoms [DRESS] syndrome).

      Six patients had brain biopsies and all showed inflammation of the brain (with B- and T-cell infiltrates), but three also contained areas of eosinophilic inflammation which is not usually found in MS. One patient has died and most of the others are significantly disabled despite treatment with steroids and/or plasmapheresis.

      Three more patients with immune-mediated encephalitis have been reported from Spain and the United States. Two of these patients have also died.

      The marketing authorisation holder of Zinbryta (Biogen Idec Ltd) has decided to withdraw this product from the European Union to protect public safety.

      Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare, potentially life-threatening, drug-induced hypersensitivity reaction

      Eosinophils are cells that are designed to kill parasites, but are also stimulated in people with allergies.

  • Finally

    Missouri Trial to Examine if Fasting Alters Gut Microbiome and Immune System of RRMS Patients in Helpful Ways

    •IF ameliorates the clinical course and pathology of the MS mouse model (EAE)
    •IF increases gut microbial diversity, alters their composition and metabolic pathways
    •Gut microbiota transfer from mice on IF led to protection from EAE in recipient mice
    •Findings with IER in MS patients partially recapitulates what is observed with IF in EAE

    Taking place at the Missouri university, the trial (NCT03539094) is expected to enroll 60 RRMS patients. Half will be randomly assigned to eat a standard Western-style diet seven days a week, and the other half to Western-style diet five days a week, with two days set aside for fasting (consuming a maximum of 500 calories each day).

    Funny today is my 500 calories (gonna eat now) Have not eat anything today



    • T regs can also switch back to being pathogenic cells…where does this leave us with T reg immunotherapy?

  • What happenened to England in the cup? They seemed to have lost steam in the second half. Anyway good showing to get to the semis.

    • Inexperience, pressure of the occasion plus they were playing a very savvy side of experienced players with 2 of the best midfielders around in Modric and Rakitic. Plus England didn't take their chances (should have been at least 2 up at half time), Croatia did.
      No disgrace though for a change 😉

  • mousedoctor
    i noticed you mentioned that the phone was causing you an issue with posting. it seems to be a browser issue on the phone as i get the same thing. try using chrome, as that solved the issue for me.

  • MGUS and MS – do you have any knowledge/opinion about monoclonal gammooathy and MS? Is it recognised and if it occurs is there an opinion on using DMTs which are usually immunosuppressive in the face of MGUS? Thanks

    • Funct Neurol. 2004 Oct-Dec;19(4):253-6.
      Unusual association of multiple sclerosis with monoclonal gammopathy of undetermined significance (MGUS): two case reports.
      Rentzos M1, Michalopoulou M, Gotosidis K, Caponi A, Bonakis A, Kilidireas K, Nikolaou C.

      There are a number of other case reports.

      Many of the agents for multiple myelma are B cell depleting agents…so I guess you can guess what I think but i'm not a neuro

  • MD2 I know that you were as frustrated as me at the bill to legalise cannabis for medicinal use not getting a reading in parliament. It had been so painful to read Andy's guest post on the issue, back in Feb, and pertinent to wife Vicky.
    Am so pleased to receive today an email from the home office in reply to signing an online petition. So good to know some progress, if limited is being made, and I hope that someone like Vicky benefit from the panel that is providing a route for specialist clinicians to prescribe cannabis based products in exceptional circumstances.
    Start of better things to come, I hope!

  • Virus and dementia 🙂

    Herpes Viruses and Senile Dementia: First Population Evidence for a Causal Link

    Abstract: Three articles have very recently appeared that are of especial relevance to the causes of dementia and its potential treatment. The first two (Tsai et al., published in PLoS One in November 2017; Chen et al., published in the January/February 2018 issue of Journal of Clinical Psychiatry) demonstrate an increased risk of subsequent senile dementia (SD) development in patients with acute varicella zoster (herpes zoster) infection. These articles present data highly relevant to the third, and most important, paper—by Tzeng et al., published online in the journal Neurotherapeutics at the end of February 2018. These authors report that infection with a different herpes virus, herpes simplex virus type 1 (HSV1), leads to a similarly increased risk of later developing SD. Further, when the authors looked at patients treated aggressively with antiherpetic medications at the time, the relative risk of SD was reduced by a factor of 10. It should be stressed that no investigations were made on subjects already suffering from SD, and that those treated were the few rare cases severely affected by HSV. Nonetheless, antiherpetic medication prevented later SD development in 90% of their study group. These articles provide the first population evidence for a causal link between herpes virus infection and senile dementia.

    Are you on the right track? 🙂


  • Please can someone explain why no-one is discussing the Coimbra Protocol properly? There are practitioners all over the world – and yet we seem to have no neurologists in the UK prepared to stick their heads over the parapet! Vitamin D seems to be relatively cheap and side-effect free (when monitored & dosed under medical supervision!) – or is that the problem – it's cheap and doesn't create more side effects – less profit for the pharmaceutical companies!
    Dr Coimbra doesn't appear to be a "quack" to me – am I missing something? The testimonials seem genuine and the results seem amazing – what is there to lose, for a patient with MS – if it doesn't work, then do the chemical drugs – it doesn't sound like he stops his patients from carrying on with their mainstream drugs if they want, but most seem to ditch them in the end. The FB community page (created by his patients!) also seems to be genuine and patients seem optimistic about their progress on the protocol – posting copies of their MRIs! I don't understand the need to keep this protocol away from the UK population – we're one of the countries with the highest rate of MS cases!
    There has been other research done within this area – – why do neurologists in the UK not even mention D3 to MS patients?
    There seems to be evidence out there pointing to the importance of vit D – why are UK neurologists not visiting Dr Coimbra and talking about his approach? Why are UK MS sufferers not even being told about the importance of vitamin D – I know someone who has had MS for 23 years and her neurologist has not mentioned vit D even once in those 23 years!
    Please explain this, as I really don't understand the apparent lack of interest or even curiosity!
    Thank you for your response in advance! 🙂

    • This is ProfGs interest not mine but there is plenty on this blog about vitamin D and the levels recomeneded. As to the Coimbra protocol I would ask where is the evidence it is useful…this is a science blog not an anecdote blog.

      Once a proper trial is done then it can be discussed.

  • It's pretty clear to me that there is a concerted effort to kill off this blog. There is very little in the way of posts relating to new research papers. The number of comments over the last few months has been minimal. Prof G hardly posts and Prof M and MD2 appear pretty much disinterested. Why not kill it off for good rather than let it suffer a slow death? I also think that MS research is in the doldrums. Has there been any really interesting research published this year. I would also been interested in finding out what Team G are up to (given that you are funded from the public purse). What are you working on and what papers have the group published this year. Where are we with the Charcot Project and with the spasticity trial? What else is on the horizon?

    • "There is very lttile in way of posts on new research papers".

      I agree… (a) Harder to find interesting papers that we have not covered before.v(b) New direction of blog administration (c) Work and Life issues.

      However, your point has been discussed.

      ProfG has been posting interesting papers on his Twitter account (Maybe you can follow him) as there has only been one blog post a day, based on the new regime.

      Do you like it or not?

      Personally, I don't. It is too ordered and the drivel posts (e.g. info posts) were taking the days post away. It has been agreed that there may be two posts if the one post has no substance.

      We will perhaps do a weekly digest of papers, ProfG volunteered but has not done this yet.

      MD & MD2 do not comment as much, as there have been less comments and much of the contensious stuff has been watered away. Google and android has locked MD from commenting by phone (hence the terrible spellin), which was often done travelling to and from work. Maybe this issue will be resolved when/if the blog moves to a new platform and "Blogger" is ditched. Its search function really is useless.

      "MS researh is in the doldrums".

      There has been less money available as the recession and austerity has taken its toll and Brexit has yet to come.

      Places like the Wellcome Trust that used to fund UK science, have decided to put more money into fewer people strangling the diversity of science. This has had a knock on effect on charites.

      Maybe they (Wellcome Trust) think they can get more nobel prizes for their buck by funding Big science and building buildings rather than supporting people in them to do cross-discipline science.

      People are being forced to do safe science rather than take a risk, that may give a big gain, because if you get it wrong your funding is cut. That is unless you are made of teflon. In which case the "Sh1 don't stick", as some science is being funded that I predict will go nowhere of importance. However they are onto the next big think before that will be found out.

      Clinical MS research perhaps has had its hayday as a number of agents are available to treat MS. This success has meant that it will be difficult to develop new treatments for relapsing MS in the future. Although the rewards are there, the costs of doing trials has got out of hand.

      As you can't ethically do placebo controlled trials means you have to pay for the comparitor drug for RRMS trials.Who has that few spare millions? Yep no-one except pharma.

      However, some pharma appear to have been divesting interest in MS, as the patents on their block busters expire. For some there is nothing new in the pipeline, having invested in turkeys. Let's see who the big players at ECTRIMS are. However where old players lie new ones will emerge.

      Has there been much interesting stuff published this year, yep there has been interesting stuff been presented. We demonstrated how cladribine works for example :-).

      I think I published more papers in 2017/2018 than ever. There are more remyelination approaches than I care to mention. However until they show some value in humans what is the point of reporting all of them

      "I would also been interested in finding out what Team G are up to (given that you are funded from the public purse)".

      I think you will find that alot of our research is not from the public purse. However we are open about what we do and what we want to do.
      As the papers are published we can discuss them. The grants and direction that we have from the public purse are all in the public domain and the papers that we have published can be found by clicking on the "About" Tab above. Scroll down to publications, Click on the person of interest and you get their publications as they are updated by Queen Mary Univeristy of London.

    • "Where are we with Charcot Project?" Inspire trial has been published not sure if stage two has been funded

      "Spasticity trial?"…Has Ipsen bought Canbex? There is the answer? Abstract has been written for ECTRIMS 2018.

      "On the horizon?" The next thing is the PROXIMUS neuroprotection study. The data is locked and is being analysed. I wonder if people took the sodium channel blocking drug..otherwise it will be a bust.

      Then there is the submission of MSChariot to the NIHR. Is the cost too much?

  • So wondering whether there will be some articles related to diet and exercise.

    I recall there being suggestion these could be considered almost DMTs in their own right, at one stage, and that a series of posts would be deicated.

    I guess I’m becoming cynical, but am wondering whether the relunctancy stems from perhaps not wanting to bite the hand that feeds you. I.e. pharma might not like focus being taken away from medication.

    I have been watching a lot of health documentaries about the benefits of a plant-based diet.

    In many of these documentaries, there is a suggestion that medical advice recommends certain dietary regimes and they ignore many obvious benefits that diet can give, and in some cases the deterimengal impact of diets we eat. Such as diary and meat.

    I have faith that the Barts team, are a bunch of very honest and ethical people. Driven by a willing to do good.

    Please use the position you are in, to demonstrate that things such as diet and exercise, can be the biggest impact to their Qol,and can do so while taking medication.

    I look back and wonder how it was possible, that when being diagnosed and obviously overweight that my physician made not comment about diet or exercise at the time.

    • "So wondering whether there will be some articles related to diet and exercise."

      From me I can say probably none, so don't hold your breathe.

      This is not where my interest or knowledge lies, I am not the person who should be giving treatment advice and importantly given that most studies on diet and excerise are of such poor quality, then I would not want to comment..You can only say "These studies are so hopelessly underpowered (because they are too small) to say anything meaningful" so many times. It has nothing to do with the fact that we conduct studies with pharma. If a certain diet creeates a cure I would be happy to post on this, but I seem to spend my time removing nonsense comments from scammers claiming such cures. In reality I suspect we are talking about incremental effects

      However it also the case that I dont have enough information to say that they are wrong.

      Advice should be based on solid science. However many diet/exercise studies are so poor I am not going to waste my time on them.

      This occurs because it costs alot of do a trial properly and as there is no profit to be made from these lifestyle issues so there is little hard science.

      N.B. However, I am sure diet and excerise are vital to health. The key is surely to have a balanced diet to help maintain health. If this come from plants fine, if they come for meat fine. We are omnivores designed to eat plants and meat.

      However, we should not be a quack medical site peddling miracle cures. There are enough of these out there (like the "5 a day" nonsesence which is just a marketing campaign) and we don't need to be one.

      Likewise there is a load of science dressed up to be something better than I am sure it will prove to be. However, they can burst their own bubble.

      Maybe one of the neuros may want to do this as part of their prevention campaign.

      Maybe ProfG will give more on diet after all he did write a forward in a diet book. Or maybe there will be a Guest post.

      As to watching documentaries on TV, beware..many of them make me cringe and it is bad pop science.

      Our physician probably made no comment on specific diets because they do not have the hard evidence to support their use.

    • Intermittent metabolic switching, neuroplasticity and brain health

      During evolution, individuals whose brains and bodies functioned well in a fasted state were successful in acquiring food, enabling their survival and reproduction. With fasting and extended exercise, liver glycogen stores are depleted and ketones are produced from adipose-cell-derived fatty acids. This metabolic switch in cellular fuel source is accompanied by cellular and molecular adaptations of neural networks in the brain that enhance their functionality and bolster their resistance to stress, injury and disease. Here, we consider how intermittent metabolic switching, repeating cycles of a metabolic challenge that induces ketosis (fasting and/or exercise) followed by a recovery period (eating, resting and sleeping), may optimize brain function and resilience throughout the lifespan, with a focus on the neuronal circuits involved in cognition and mood. Such metabolic switching impacts multiple signalling pathways that promote neuroplasticity and resistance of the brain to injury and disease.


    • "We are omnivores designed to eat plants and meat."

      You are a scientist! We were not designed, we evolved. While eating meat, or rather the social demands of hunting, may have influenced our evolution, I am not sure that there is any solid scientific evidence that we require meat in that it promotes health, longevity, brain development, intelligence etc.

      It's certainly not essential for muscle development. Look at a silverback gorilla.

    • As a layperson from the UK, who considers the NHS as uber conservative, it is quite something to see the webpage on intermittent fasting. The NHS refers to 'animal research as striking' and adding 'Prolonged nightly fasting maybe a simple, feasible and potentially effective disease prevention strategy' It references reducing risk of chronic conditions such as cancer, diabetes and obesity.
      As I've read on other sites, the English word for the first consumption of calories each day being 'breakfast' means exactly that – breaking your fast.
      The NHS says there's no studies on the optimal duration of nightly fasting, but my attitude is that it clearly don't hurt and is easily achievable. I'm comfortable doing anywhere between 12/12 and 14/10. If there's any chance of it being of benefit cognitively as well as physically I'm even more chuffed to have adopted this approach to daily eating and drinking.
      Hope anyone else trying it finds it as easy as I have!

    • "Its not essential for muscle development"…I know I eat vegetarian muscle all the time:-)

      If you don't believe in evolution can you be a scientist?

    • "If you don't believe in evolution can you be a scientist?"

      You can be a scientist who has as yet failed to grasp the incredible wealth of scientific evidence for the theory of evolution. NB: It is not necessary to "believe" in evolution.

  • Brain Iron Levels Correlate with MS Progression, Disability Risk, Study Shows

    Evaluating the local differences in iron accumulation in the deep gray matter of the brain using a special magnetic resonance imaging (MRI) technique, may help identify multiple sclerosis (MS) patients at greater risk for disease progression and disability, a study reports.

  • Molecular Key for Delaying Multiple Sclerosis Progression

    In the work just published it was possible to identify a receptor known as P2X4 present in the microglial cells that increases their anti-inflammatory potential in order to reduce the damage in Multiple Sclerosis and, above all, encourage the body's own repair responses.

    This experimental development was conducted using animal models of this disease, thanks to which it was possible to discover that the drugs that activate this receptor improve the symptoms during the chronic phase of the disease when furthering the repair of the nervous tissue.

    [It finally seems that the scientific community is on the right track about progressive MS. A lot of research is going on about the innate immune system, from MS and Alzheimers to depression. There is a lot to learn there.]

    • Please read the post on this paper, If we think that animal disease of a few days is progressive MS that evolves over months and years, we are probably deluding ourselves.

  • "a very savvy side of experienced players with 2 of the best midfielders around in Modric and Rakitic."

    MD2 World Cup is over..back to the lab you go before you talk like TV soccer analyst permanently..and not a scientist.

  • What do you think about MS heterogeneity: Four lesion patterns, different responses to medication, IgM present only in 50% of the patient's oligoclonal bands, etc.

    Is it possible that we are dealing with different diseases?

    • The 4 patterns were seen in biopsies but in post-mortem there was homogeneity and two of the lesion types were not really seen.

      "Is it possible we are dealing with different diseases", sure it is possible. Until recently NMO was called Devics MS, but there is now evidence for an antibody component a differnt pathology and a different response to therapy. Maybe we will be able to find certain groups of people that respond in a certain way.

  • A new roadmap for repairing the damage of multiple sclerosis

    "We were shocked to find that almost all of these previously identified molecules share the ability to inhibit specific enzymes that help to make cholesterol. This insight reorients drug discovery efforts onto these novel, druggable targets."

    Using a new 3D nerve cell culture model that resembles human brain tissue, the researchers confirmed their findings in the laboratory, showing that the therapy candidates promoted myelin formation by blocking enzymes in the cholesterol pathway.

    Convelo Therapeutics new platform will focus on developing therapies for myelin regeneration in neurological diseases such as MS.



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