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MouseDoctor

79 comments

  • Two part question:

    1. For those of us on B-cell depleting therapies (rituxumab, ocrelizumab), do you think there would be any utility to be on an antiviral such as valacyclovir or famciclovir to suppress EBV spread? I figure it would work well theoretically since we are destroying most of the EBV reservoir in the B cells.

    2. I was thinking of adding on betahistine (a benign antivertigo drug) as a H3-antagonist for remyelination based on this study:

    http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0189380

    GSK's candidate H3 receptor antagonist GSK239512 has shown success in remyelination (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306088/) so I figure betahistine would also work. Thoughts?

    • Anybody on therapy is on a B cell depleting therapy, some are just better at it than others.

      We dont recommend off-label use of any agent. Drugs interact with each other and this needs to monitored properly to ensure safety.

      Ask your neurologist

  • Are you seeing any additional and unexpected side effects emerging following use of oral Cladribine, other than those already listed? Do you think it could potentially be as effective as Alemtuzumab and without secondary autoimmune diseases? Any promising signs so far of actual improvement in advanced patients or at least disease stabilization?

    • Early days for Mavenclad. So far no safety signal. Could it be as effective as alemtuzumab? In highly active disease Cladribine results are impressive, however alemtuzumab has more robust (phase III x2) and long term (NEDA, atrophy) data. The problem of autoimmunity with alemtuzumab has been insufficiently addressed; it does not occur with cladribine.

    • Are you joking? Cladribine causes lymphopenia, herpes simplex and zoster infections. Of course there is a safety signal.

    • Apologies, no *new* safety signal. Cladribine works by inducing a selective lymphopenia, so no surprise you find this in people taking it, but nowhere near alemtuzumab, where grade 4 is the rule. The rate of infections is modest, again well below equivalent DMTs.

    • Going in the results from your Sience Direct Publication, what are the next steps? Is a more robust study planned to show usefulness of Mavenclad for SPMS disease patterns?
      Do you think it will be approved one day for treatment of SPMS?

    • Reading DrK's positive comments here about Mavenclad makes me wonder why on earth anyone would choose to take Alemtuzumab or Natalizumab with their potentially far more serious long term side effects. I sincerely hope Mavenclad soon becomes widely available to all patients with MS – it seems so unjust that it isn't already.

    • I realize we don't yet know long-term safety of Cladribine but I personally had more side effects when taking painful daily Copaxone injections than when taking the Cladribine tablets.

    • We've submitted #ChariotMS to the NIHR, and first crunch time is this month. Will the panel see the same value as we do in treating pwMS who have an EDSS of 6.5 or above? Mavenclad would have evident advantages in terms of convenience/transport since people can take drug at home, but failing that we would need to use a generic. Anyone's guess where the manufacturer will go next (or go at all?) in terms of progressive MS in EDSS 6 and below.

    • Viral infections…through dose and lymphopenia monitoring we may be able to reduce unwanted viral infections

    • Didn't one study show that just 40% of people who took Mavenclad (Cladribine) had NEDA after two years? And haven't doctors on this site said that you've seen (serious?) rebound relapses on people treated with Mavenclad? Maybe Mavenclad is just much less effective than the other PIRTs.

    • Didn't one study show that just 40% of people who took Mavenclad (Cladribine) had NEDA after two years? And haven't doctors on this site said that you've seen (serious?) rebound relapses on people treated with Mavenclad? Maybe Mavenclad is just much less effective than the other PIRTs.

      The number is 47%, and the corresponding figure for NEDA in CARE MS 1 was 39%. No rebound with cladribine, this is largely a feature of the blocking/sequestering agents natalizumab and fingolimod.

  • What's the most recent news regarding NICE and Ocrelizumab for RRMS? Do you think it'll be much longer before its approved? I've just been told I'm JC positive so can't stay on Tysabri for much longer. I'm hoping to go onto Ocrelizumab so I wish NICE would hurry up.

  • The latest research by Dr. Anette Christ and Prof. Eicke Latz has shown that a ‘Western Diet’, rich in refined sugars, salt and saturated fat, activates the immune system similarly than a pathogenic infection

    http://www.iii.uni-bonn.de/nc/en/press/press_view/article/western-diet-induces-inflammation-and-trained-immunity.html

    http://www.iii.uni-bonn.de/nc/en/press/press_view/article/western-diet-induces-inflammation-and-trained-immunity.html

    Beware of the pizza atack….. 🙂

  • Is there any evidence that diary should be avoided, for pwMS? Are there any foods that inparticulaly, should be avoided by pwMS?

  • I have an unrelated question. I was dx in 2012 with progressive MS (neuro wavers between SPMS and PPMS as I had CSI (optic) in 1984 then absolutely nothing until c2005/6 and progressive deterioration w/o relapse ever since). A blast of steroids in 2012 did no lasting good. I take self-funded Fampyra and biotin and also simvastatin. I see neuro once a year (at best) which consists of quick chat to check I am still alive. Have had no follow up MRI since 2012 and no other investigation or treatment of any sort. I read all the material here about Cladribine, Ocrelizumab et al and how you appear to actively monitor and treat your patients and wonder if I am living in another world. What should I be asking my neuro to do?

    • Refer you to a neuro who will actively monitor your condition?

      I am sorry we can't give individual advice on the blog, so please don't be uset if the neuros don't respond

    • Peter – I was in this situation and considered the three options available to me at the time:

      (1) stick with what neuro contact you have and take a passive role in your treatment; what you describe as the annual meeting and then inactivity seems to occur quite widely according to the people I meet and talk to in the MS Centre.

      (2) arrange another meeting with your neuro and ask them to find out if/how you are progressing and if you have current disease activity, and ask them to consider/recommend suitable treatments for you.

      (3) As MouseDoctor suggests, seek a referral with another neuro. To do this go to your GP, say that you are unhappy with the different diagnoses you have received concerning your condition and the lack of treatment options offered to you by your current neuro, and ask them to refer you to another hospital/neuro. Your GP will probably report that that (a) other consultants don't necessarily have to accept you as a patient, (b) may give you exactly the same diagnosis and treatment options (i.e. none) as your existing neuro, and (c) in the UK it is more likely to be accepted by another neuro at a hospital in the same NHS region due to the regional funding arrangements. They may also tell you that leading authorities in MS
      will be less likely to accept you as they will invariably get lots of referral requests and may not have capacity to take on any more.

      I started with option (1) but quickly realised this was not for me. I then did option (2) but got nowhere. I tried (3) about 2 years ago and I'm now with a neuro at another hospital and have not looked back since. I'm still a patient with my original MS nurses from the old hospital, but now have a non-local neuro at another hospital. This causes hassle with travel arrangements when I have to meet my neuro, but this is a small problem in the big scheme of things. Under the new neuro I initially had a battery of tests (MRI, LP, bloods galore) and then had another meeting to discuss treatment options and how to manage my condition. If I had done this 2 years earlier, I could have started DMT 2 years earlier than I did….

      Good luck –

  • MD could you talk about it?

    TOX, a DNA-binding factor that may play a role in triggering multiple sclerosis – the team reports that TOX allows cells to cause autoimmune damage to brain cells.

    They used two different pathogens – one viral and one bacterial – that are known to elicit a response from the immune system. The research was performed using healthy rat models. According to co-author Nicolas Page, a researcher in the Department of Pathology and Immunology at UNIGE, both pathogens elicited an "identical quantitative immune response" from a certain type of white blood cells: CD8 + T lymphocytes.

    Was this the reason for the causal link between EBV and MS?

    https://www.cell.com/immunity/fulltext/S1074-7613(18)30142-0

  • Researchers transform human blood cells into functional neurons

    Somewhat mindboggling

    "It's kind of shocking how simple it is to convert T cells into functional neurons in just a few days," Wernig said. "T cells are very specialized immune cells with a simple round shape, so the rapid transformation is somewhat mind-boggling."

    Converting T cell into neurons? ……….UAUUUUUUUUU

    https://medicalxpress.com/news/2018-06-human-blood-cells-functional-neurons.html

    Transdifferentiation of human adult peripheral blood T cells into neurons

    http://www.pnas.org/content/early/2018/05/30/1720273115

    Obrigado

    • Will you comment?

      "Another important scientific finding of the studies, Zivadinov continued, is that atrophied brain lesions were a more robust predictor of disability progression than the development of whole brain atrophy itself, the most accepted biomarker of neurodegeneration in MS.

      “Our data suggest that atrophied lesions are not a small, secondary phenomenon in MS, and instead indicate that they may play an increasingly important role in predicting who will develop a more severe and progressive disease,” he said."

  • When will there be better medication for nerve pain? Having tried all of the "standard" anti-epileptic drugs/anti-depressants etc that are used for neuropathic pain, nothing is left. I feel this is an ignored area of MS; having 24 hour pain that is uncontrollable is not survivable, yet it's not seen as a problem. Any thoughts?

  • At Haukeland University Hospital, Bergen, Norway, they seem to be recruiting for a head to head study (RAM MS study) of alemtuzumab versus autologous stem cell transplantation. Here is a google translate version of the project homepage (in Norwegian). Has somthing similar been done before? Any thoughts?

    About the RAM MS study:
    This project aims to investigate whether there is a difference in treatment effect, safety and cost between autologous stem cell transplantation and best approved MS drug (alemtuzumab).

    In Norway, around 6000 people have registered with MS. Up to now, approximately 30 MS patients have been treated with autologous stem cell transplantation in Norway, and a larger number of Norwegian MS patients are treated with the drug alemtuzumab (Lemtrada®) each year.

    Autologous stem cell transplantation is not approved as standard MS treatment in Norway, and no study has been done to compare the effect of these two MS treatments. It is planned that approx. 100 patients will participate in the study. The study is approved by the Regional Committee for Medical and Health Research Ethics and the Norwegian Medicines Agency.

    Patients who may be relevant to the study should be referenced from their treating neurologist to the regional study center for review of inclusion and exclusion criteria and randomization to the study.

    Detailed information about the reference can be found under the "For Patients and Relatives" and "For Health Care" tabs.

    Inclusion Criteria:

    1) Attakk during ongoing MS treatment last year, treated with steroids and verified on MR.
    2) MR: At least 1 contrast-laden lesion or at least 3 new or enlarged T2 lesions.
    3) Age: 18-50 years.
    4) RRMS after revised McDonald criteria.
    5) EDSS 0 to 5.5.
    6) Attaked / attaks must have occurred> 3 months after initiation with immunomodulatory medication.

  • Identification of a critical sulfation in chondroitin that inhibits axonal regeneration

    The failure of mammalian CNS neurons to regenerate their axons derives from a combination of intrinsic deficits and extrinsic factors. Following injury, chondroitin sulfate proteoglycans (CSPGs) within the glial scar inhibit axonal regeneration, an action mediated by the sulfated glycosaminoglycan (GAG) chains of CSPGs, especially those with 4-sulfated (4S) sugars. Arylsulfatase B (ARSB) selectively cleaves 4S groups from the non-reducing ends of GAG chains without disrupting other, growth-permissive motifs. We demonstrate that ARSB is effective in reducing the inhibitory actions of CSPGs both in in vitro models of the glial scar and after optic nerve crush (ONC) in adult mice. ARSB is clinically approved for replacement therapy in patients with mucopolysaccharidosis VI and therefore represents an attractive candidate for translation to the human CNS.
    https://doi.org/10.7554/eLife.37139.001

    Obrigado

  • I live in the Netherlands, and have asked my dr about monitoring subclinical disease activity beyond traditional MRI. More specifically, I would like to be monitored on biomarkers such as brain volume loss, and neurofilament levels. My doctor says that these are only utilised in research, as they are not relevant to clinical practice at the moment.

    The content of your blog indicates otherwise. Do you measure these at your hospital? Are they integrated into clinical practice in the U.K.? If yes, could I maybe get in contact with you and have these measurements performed?

    Thank you beg for your reply

  • Just wanted to say I've started on Metformin with Clemastine to get some remylination going after seeing this


    and reading this
    https://www.neurologyadvisor.com/multiple-sclerosis/metformin-pioglitazone-anti-inflammatory-effect-in-ms-patients-with-metabolic-syndrome/article/485829/
    (Many thanks to the people who originally posted these very exciting links.)
    At least I hope I'm taking Metformin – my neurologist is fine with me having it but too busy to send the promised letter to my GP so I've had to get it from Canada (poor overworked neurologists).

  • Hi

    I wanted to ask about the cooccurrence of Graves disease with thrombocytopenia after alemtuzumab. It seems that the two might go hand in hand. Is there some similarity between autoimmune thyroid and platelet antibodies?

    I had severe ITP 2 years post alemtuzumab that continued relapsing and was non-responsive to steroids. Six months after initial ITP onset severe graves disease became apparent and the ITP started relapsing severely (platelet count <5). Eventually I had a thyroidectomy, a course of rituximab to calm the B-cells, and a drug called eltrombopag to promote platelet growth (as an alternative to a splenectomy), and it seems to have sorted things out. Thankfully my MS has remained quiet through all of this.

    There has been another case written up very similar to my own http://www.bloodjournal.org/content/130/Suppl_1/2326 – this person also had rrMS, Graves, and ITP. Please note that the huge rebound effects seen were avoided in my case by carefully monitoring platelet levels on a daily basis and stopping eltrombopag immediately once they reached 300.

    I feel like these issues will become more and more apparent as the numbers on Alemtuzumab increase, and it's important that they're properly tracked. It's also interesting to consider what this might mean for my future treatment options should I need them.

    • Can prof g please answer this as following lemtrada I also have thyroid problems so I'm concerned by this particular entry

    • I am sorry to say ProfG is unable to answer specific questions.

      However, ITP and Graves has been reported previously

      Adrouny A, Sandler RM, Carmel R. Variable presentation of thrombocytopenia in Graves’ disease. Arch Intern Med. 1982;142:1460

      Valenta LJ, Treadwell T, Berry R, Elias AN. Idiopathic thrombocytopenic purpura and Graves disease. Am J Hematol. 1982;12:69

      Kurata Y, Nishioeda Y, Tsubakio T, Kitani T. Thrombocytopenia in Graves’ disease: Effect of T3 on platelet kinetics. Acta Haematol. 1980;63:185–90.

      Cordiano I, Betterle C, Spadaccino CA, Soini B, Girolami A, Fabris F. Autoimmune thrombocytopenia (AITP) and thyroid autoimmune disease (TAD): Overlapping syndromes? Clin Exp Immunol. 1998;113:373–8.

      Cheung E, Liebman HA. Thyroid disease in patients with immune thrombocytopenia. Hematol Oncol Clin North Am. 2009;23:1251–60.

      Gill H, Hwang YY, Tse E. Primary immune thrombocytopenia responding to antithyroid treatment in a patient with Graves’ disease. Ann Hematol. 2011;90:223–4.

      Hofbauer LC, Spitzweg C, Schmauss S, Heufelder AE. Graves disease associated with autoimmune thrombocytopenic purpura. Arch Intern Med. 1997;157:1033–6.

    • Thanks for answering this – it seems that these issues have been documented for quite a while. My medical team seemed to have belatedly decided that it was the graves causing the ITP, but they were pretty reluctant to make the link at the time.

      A couple of final thoughts that might be worth incorporating into future monitoring
      – in Australia's bloodwatch lemtrada monitoring system thyroid issues are only checked every 3 months (and it only looks at TSH levels, not free T3 T4 or antibodies)
      – when I first got ITP we had no recent thyroid checks done, although I had lost a bit of weight which I put down to exercise. They didn't check me for thyroid issues when I presented with ITP, they gave me steroids and waited it out

      – It wasn't until 5 months later that bloodwatch picked up my graves disease (less than 4 weeks after I finished tapering off steroids), and a couple of weeks later the ITP relapsed.

      – I'm almost certain I had graves disease grumbling along the entire time that may have been masked by the high dose steroids I was put on for the ITP. If a proper screen for graves had been done perhaps we might have caught these issues earlier and I could have avoided multiple hospitalisations for severe recurrent ITP

      – So perhaps it should be standard practice that anyone presenting with ITP post lemtrada should also be checked for thyroid antibodies. I don't think it is too much of a stretch to suggest that it could be life saving.

  • Are there any current trials for the impact of intermittent fasting on MS?

    I saw a post on your twitter updates, and I wondered whether you can advise on any inflight trials, and when we can anticipate results?

    In the meantime, I’m trying to do a 12pm-8pm eating, remainder of the time fasting. As it’s not so difficult and i think there are obvious health benifits which will help general health regardless of the impact on MS

    • "a commonly prescribed drug that mimics the effects of fasting, namely Metformin."

      Do you know how it does this..?

    • Metformin's main effect is to decrease liver glucose production. It is used by type II diabetics. Apparently it acts to promote rejuvenation of oligos

    • The guy giving the (appropriately named) Stop MS lecture (at https://stopms.mssociety.org.uk/annual-lecture.html ) goes into quite a lot of detail about what intermittent fasting does and how Metformin mimics this. Start watching at 33.33 for this bit. Metformin and fasting improve NPK(?) signalling, which slows as you age. NPK signalling makes stem cells responsive to turning into oligodendricites which do remylination on nerves where the myelin has been damaged (I think – watch the lecture to see if it says the same thing to you)..
      I have been on Metformin for a week and I can now get into bed at night without help (I haven't been able to do that for a few months). Really hoping it's the Metformin but have no idea whether this is too quick to see effects.

    • Fasting

      Downregulates the mTOR pathway which is responsible for

      cell growth, cell proliferation, cell motility, cell survival, protein synthesis, autophagy, and transcription…etc

      Central nervous system disorders / Brain function

      Alzheimer’s disease
      mTOR signaling intersects with Alzheimer’s disease (AD) pathology in several aspects, suggesting its potential role as a contributor to disease progression. In general, findings demonstrate mTOR signaling hyperactivity in AD brains. For example, postmortem studies of human AD brain reveal dysregulation in PTEN, Akt, S6K, and mTOR.[80][81][82] mTOR signaling appears to be closely related to the presence of soluble amyloid beta (Aβ) and tau proteins, which aggregate and form two hallmarks of the disease, Aβ plaques and neurofibrillary tangles, respectively.[8

      ] Intermittent mTOR activation in prefrontal neurons by β-hydroxy β-methylbutyrate inhibits age-related cognitive decline associated with dendritic pruning in animals, which is a phenomenon also observed in humans.[116]

      Scleroderma, also known as systemic sclerosis, is a chronic systemic autoimmune disease characterised by hardening (sclero) of the skin (derma) that affects internal organs in its more severe forms.[118][119] mTOR plays a role in fibrotic diseases and autoimmunity, and blockade of the mTORC pathway is under investigation as a treatment for scleroderma.[8]

      Obrigado

    • "Start watching at 33.33 for this bit"
      THANKs..must missed it when I watched.

      But don't you need to take something like Clemastine
      to go with the Metformin..?

    • Has anyone tried the 8 hours food-16 hours fasting type of diet? It is a daily kind of fasting that is supposed to help autophagy too. Can't find any reference for MS though.

    • I on it for more than a year now,

      Also do 5:2 diet

      Watch this presentation he talk about 8 hours food-16 hours fasting type of diet also Ms

      Obrigado

    • "Yes, the idea is you take Metformin and Clemastine"

      How long and how much are you taking of each..?

  • Discovery shines light on the mystery of cell death in multiple sclerosis

    Pyroptosis is a type of programmed cell death that is associated with inflammation, but its role in MS was previously unknown. Importantly, Power's lab was able to show pyroptosis in both brain tissues from MS patients and in lab models of MS.

    Power's lab found that the drug known as VX-765 protected oligodendrocytes, the cells that insulate nerves in the brain and are susceptible to damage in MS. VX-765 is currently in clinical trials for epilepsy.

    "We think this drug would break the cycle of neurotoxic inflammation and thus prevent future loss of brain cell in MS," said Brienne McKenzie.

    https://medicalxpress.com/news/2018-06-discovery-mystery-cell-death-multiple.html

    http://www.pnas.org/content/early/2018/06/11/1722041115

  • Any advice please on where I could go online for a tutorial on B cells & immunology?

    Basically, Id like to learn more about

    (1) the impact of fasting on memory B cell numbers? If they normally live decades does fasting kill them?
    (2) the impact of Vitamin D on EBV & memory B cells?
    (3) the process by which naive mature B cells are activated into memory B cells? At what point to they become infected?
    (4) the impact of exercise on neuroprotection of the whole brain- not just the hippocampus.

    • "The proof is in their bank account"

      2 Stock offerings just this year alone raised
      over 200 million..so Phase 1,2 and 3 of
      allogeneic ATA 188 are guaranteed to finish.

    • http://nn.neurology.org/content/5/4/e466

      "Previous studies attempting to demonstrate EBV in the MS brain observed the presence of EBV-infected B cells in lymphoid-like B-cell follicles.3 These initial studies were challenged by the inability of different groups to consistently identify EBV-infected B cells in cortical structures such as meningeal follicles with germinal centers.
      We were also unable to identify any lymphoid-like structures in the tissue we examined, leaving open the question of whether such structures exist and whether meningeal B-cell follicles represent an important site for accumulation of EBV-infected B cells in the MS brain."

    • Thanks.

      If we look at lymph nodes we find the antibody cells, whilst made in the follicles do not reside in the follicles. Therefore I suspect the B cell follicle in MS is the wrong place to be looking for these things.

      BenJ has done a post on this paper. It will apear soon

    • The news story was about CD8 T cells being used as an EBV vsaccine. They plan to use allogeniec cells (i.e cells from another person) so they start to throw immune theory out of the window.
      Whilst the original Pender idea I can buy this idea is Dubious.

    • "Does the big Pharma is "waking" and solving look at this way?"

      Cinara Atara Bio would not really be a big Pharma..as they only
      exist for 6 years or so and have never had a licensed therapy or a single $ in revenue. Their EBV Tcell therapies for EBV cancers will be first..but based on the potential for their
      MS therapy they sold over 200 million in stock this year giving
      them 400 million in total reserves. Stock Investors know that
      MS = $$

    • But it's already a "sigh" about looking at EBV and MS, since most MS drugs are only potent immunosuppressants.
      And yes, unfortunately, money is the hand that moves the world.

  • BCG vaccine leads to long-term blood sugar improvement in type 1 diabetes patients

    Long-term follow-up of participants in clinical trials of a generic vaccine to reverse advanced type 1 diabetes finds significant clinical benefits, including restoration of near-normal blood sugar levels. Three years after receiving two administrations of the bacillus Calmette-Guérin (BCG) vaccine four weeks apart, all members of a group of adults with longstanding type 1 diabetes showed an improvement in HbA1c to near normal levels—improvement that persisted for the following five years.

    https://medicalxpress.com/news/2018-06-bcg-vaccine-long-term-blood-sugar.html

    *BCG vaccine has been and will be again under trial for MS in Italy

  • Ms epidemic?

    Take your own conclusions
    The age-at-onset analysis determined that, although all age groups and sexes experienced a positive local drift, women aged 50-64 had the highest relative increase in incidence between the decades. The study suggests that a reason for an increase in incidence is the introduction of new diagnostic criteria and tools, including magnetic resonance imaging.

    The study concluded that the incidence of late-onset multiple sclerosis more than doubled among the female population, but only showed a modest increase among men. The contribution of established risk factors is still quantitatively unknown, and delayed pregnancies along with a decrease in exposure to hormone therapies should be further studied as late onset multiple sclerosis rises in women over 50.

    http://www.neurologyadvisor.com/multiple-sclerosis-advisor/long-term-incidence-ms-pattern-development/article/775460/?utm_source=newsletter&utm_medium=email&utm_campaign=na-spotlight-20180625&dl=0&DCMP=EMC-na-spotlight-20180625&cpn=&hmSubId=&hmEmail=VHU0u6r2Q_Y1&NID=&dl=0&spMailingID=19784911&spUserID=NDMyMTYxNjMwMzI0S0&spJobID=1281225238&spReportId=MTI4MTIyNTIzOAS2

    Obrigado

  • 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?

  • Progression of regional grey matter atrophy in multiple sclerosis

    Across the board 🙁

    https://www.ncbi.nlm.nih.gov/pubmed/29741648

    This study was not designed to investigate the effects of
    disease-modifying drugs and comorbidities on the atrophy
    stages. However, it does study the sequence of regional
    atrophy in the presence of these confounders. There were
    no significant differences at baseline or during the followup
    in the event-based model stages of patients who were
    receiving disease-modifying treatments and those who were
    not, extending our previous results in the same group of
    patients which demonstrated, using a different imaging
    analysis method, that the rates of atrophy in neuroanatomical
    regions were not confounded by disease-modifying
    treatments (Eshaghi et al., 2018). Most of the patients
    were receiving the injectable first-line therapies (interferon
    beta and glatiramer acetate), whose effects on atrophy rates
    are weak

    So much so the the interferons

    Obrigado

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