Q&A May

Q
Angel Fish Sculpture from the East End of London

Disclaimer: Please note that the opinions expressed in the responses below are those of the MS-Blog writer and do not necessarily reflect the positions of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust

About the author

MouseDoctor

134 comments

  • What is the name of the institution ( or the name of the researcher ) doing the HAART trial for ms in Boston ?

  • When im on steroids im pretty much symptom free, as soon as i come off them all my symptoms come flooding back. Its been like this almost a year now and ive had four lots of high dose and am currently on a low trailing dose. can my brain really still have that much inflamation ?

  • I am a PPMS patient on ocrelizumab few months shy of getting his second dossage.
    I have a question that occupies my mind:

    Let’s say that starting with a double dosage of ocrelizumab is the way to go. How long before the window of opportunity/benefit closes?
    Does it make sense to give patients a double dose of ocrelizumab while they are on ocrelizumab for let’s say 2 years or more?

    Thanks in advance

  • Assuming that covid is endemic by now, I would very much like to read an in depth discussion about the pro and cons of switching away from anti cd20 treatments (and what to switch to….) given the vaccine issues…

    • This is an interesting question….but I’m in enough trouble already and I’m not a neuro…but it is a good question. COVID-19 I suspect has had impact on which anti-CD20 and which S1P1 modulator is used, it would be good to see sales over 2020…I have my views but cant give them.

  • I Sold My Roche Stock (RHHBY)

    I am not a stock “gambler”, but seek dividends from stable stocks that go up in value over time, thus beating inflation. I bought it because I thought Ocrevus would be a big deal. I went on Ocrevus myself. Then covid. I got off the O-Train early. Appears I have antibodies now, so I’m happy (MS is about the same, clinically, I’m 63).

    But Roche (in my opinion) continues to be way too quiet about potential consequences in the covid era. There are users and even new users who are or were not properly informed of all the unanswered questions. Many are not happy. That’s my opinion based on blogs that I read.

    So I sold my stock (a 10K investment). I made some long term money and got a 3% dividend while I waited.

    But this blog is about questions, so, what is my question? Did I put my $ where my mouth is? I think so

  • If someone after first Ocrelizumab gets worse (because of existing damage that had been done over the years), how can we know whether other damage won’t re-appear after subsequent doses? Is there a potential biological mechanism involved that could explain this?

  • There are a number of HSCT trials kicking off shortly which may make it easier to access on the NHS of it is shown to be a cost effective and efficacious treatment (we probably already know this to be true). However, are there other drugs in the pipeline…the btks for instance that could prove derail the hsct train before it has really got going?

  • Have you got your eye on any new treatments for highly active RRMS on the horizon? Thank you!

    • Several BTK inhibitors are in phase 3 trials basically they stop B cells from activating as well as microglia.

  • The March 2021 edition of the Journal of International Medical Research contains an academic paper titled “HIV infection and multiple sclerosis: a case with unexpected ‘no evidence of disease activity’ status”. An MS patient saw his condition substantially improve following subsequent HIV infection and treatment. The patient achieved No Evidence of Disease Activity (NEDA) without any MS disease-modifying drugs and continues to have no disease activity more than ten years after first diagnosed with MS. The authors speculate that antiretroviral therapy, which the man is still taking for his HIV, may be responsible for his MS “disappearing” with the HIV medication perhaps treating MS (EBV in MS) as well. Should a combination of HAART drugs like the ones this case study was on (he was not on a monotherpapy) be included in the Octopus study – perhaps combivir which contains two HAART drugs?

  • How exactly is EBV thought to be the “cause” of MS? Is the idea that people get EBV, create anti-EBV antibodies, then something happens to the BBB to allow those antibodies into the CNS, and those anti-EBV antibodies act as double agents to attack myelin that happens to be partially similar to a part of EBV?

    • There are many theories on how EBV causes MS, but nobody actually knows. What I can say is that people who are EBV negative don’t get MS, which is why we have to do an EBV vaccine prevention trial.

  • Are there any studies on the effect of HSCT (or any other high efficacy DMT) on the rate of spinal cord atrophy ? And in general if a certain DMT is able to slow the rate of brain volume loss would that apply to the spinal cord as well?

  • MD1 – How are you doing?

    What is your blog status….1) probation, 2) banned, 3) starting your own blog, or 4) staying put, just now neutered?

    Hope you and the rest of the Barts team are doing okay. Wishing you all the best!

    …….I start course one, year one this week🤞

    • At the moment ProfG/K are hoping the existence of the blog has been saved but we will be getting a make-over very soon at the very least.
      I am on (1) self-imposed probation but seems like (4) if likely, but I am turning my scrotum into a gift:-)

      • Good to have this update MD – if still somewhat jittery around the uncertainty.
        Not sure I like the sound of a ‘makeover’ or the thought of your vulnerable nether regions!
        If things do go horribly, then I hope you, ProfG and others in the team will continue this blog in a different guise, independent of anything Bart’s coz we so, so need it!

        • Until a line is drawn under this…sorry to say there is uncertainty

          Howeverm, we have always been independent of Barts and the Blog is run on software and hardware outside of the university, which means we have no support…..legal or otherwise. However, people believe that this is an official University blog and it is clear that we need to make this clear that we are not and so we are making changes. We have no staff we have no-one to write or check posts, no editor, no lawyer, no money. We recieved nothing for doing this and the time we spend is our own time…for example today is a national Holiday for the Workers (Mayday).

          As for the nether regions, I am afraid it is something that needs to be done. “https://www.sciencemag.org/news/2017/11/10-million-lawsuit-over-disputed-energy-study-sparks-twitter-war”

          • If it goes horribly wrong I am toast, but ProfG will keep going I think

  • Question 1. Post Polio Syndrome, a propotion of patients with a history of spinal cord Polio infections experiencing muscle weekness ~30 years after the infection. Is this a similar cause of MS worsening after few decades with no evidence of relapses? What is lost? Demylinated neurons dying early?

    Question 2. For pwMS on anti CD20+ therapies, would inactivated vaccines a better choice theoretically? As these vaccines triggers less antibody-dependent immune responses? (I’m not asking for vaccine recommendation but if the theory has any grounds.).

    • 1. I dont know
      2. Inactivated vaccines have the advantage of making immune responses against proteins other than Spike. It seems CD8 T cells in a natural infection particularly react to nucleocapsid. However the aim of inactived vaccine is to make an antibody reponse too

  • Title of my comment: TUDCA
    Background: 3 yrs ago I had surgery on spine. I woke with right leg paralysis & severely deficient strength in left leg along with many other nerve type issues. I was in a nursing home & sent home pretty much wheelchair dependent. I was also on a ton of meds some pretty darn strong & high dosage. I had no new lesions & even though the nerve signal testing done during surgery showed nothing, it was determined that I had nerve irritation. (It was way more). I have not regained full function. I took myself off most of the meds because they all had side effects of making me sleep. The few I stayed on, I reduced to a manageable level. Upon testing at my gp, my liver values were through the roof. I felt like leg swollen and I just felt like death. Someone on my friends find a kidney page was talking about TUDCA. I looked it up & decided to try it to get my liver enzymes down. It worked. It brought my liver values down. It also seemed to help with feeling & strength in leg & energy. I stopped taking it after a while when I started feeling better due to cost. I swear that was the one helpful thing besides my pure will power to move & my recumbent bike. Then today I see something as I was reading up on it that it may be helpful for MS & that there is a trial going on now. Do you have any knowledge of the use of TUDCA in MS patients for nerve remyelinating & reducing nerve damage in MS?

  • For the purposes of computing one’s risk of developing PML while being treated with Tysabri and JCV+, would you consider a brief treatment (1-3 months) with Tecfidera and/or Aubagio to be sufficiently significant such that a patient is considered “having previously taken an immunosuppressant” ?

    Is it even possible to pass judgement on these therapies as potential risk factors given that the patient register for this analysis was evaluted in 2014 i.e. a time where Tecfidera or Aubagio had barely entered the market.

  • Attack duration – it appears to me most attacks are acute and last for days only, at most a couple of weeks. But occasionally I read some attacks last for a Month or even Months. What is the implication of duration of attacks? Do longer attacks predict progressiveness of disease course? Is there a relation between duration and recovery? (Guessing longer attack usually means poorer recovery?). Pathological differences?

    • This is complicated by age and reserve. The younger you are the more likely you are to recover. Similarly, the less damage in a pathway the more likely you are to recover. Other issues relate to the size and location of the lesion and the biology of the lesion. If the lesion becomes a SEL (slowly expanding lesion) then recovery is poor; in fact, the disability may recover but then likely to get worse.

  • Does breastfeeding merely delay the risk of a postpartum relapse or does it decrease it. My neuro said there was a ‘complex formula’ to work it out but didn’t appear aware of its detail or application! Thanks

  • Diagnosed 11 years ago, treated with alemtuzumab from beginning. I always assumed that I must be EBV positive. A recent routine full blood count tells me “EBV DNA not detected by PCR”. Has the alemtuzumab washed away the EBV virus and if so, what else could it have washed away e.g. childhood viruses?

    • Not a doctor – according to Ide, and MD’s posts on S1P modulators, Ozanimod will blunt the immune response made by the vaccines, one is very unlikely to make anti-body response (only ~3% of people compare to health/treatment-naive controls do). But the vaccine will still train part of one’s immune system, so vaccines will work, but poorer, compared to other DMTs. This is based on currently available information.

      • Data is available for fingolimod I am not aware of vaccine data for Ozanimod. It is clearly needed. One major difference is that ozanimod does not target S1P3 and this is apparently involved in B cell activity. I am not aware about T cell activity with any of the S1P1 modulators yet.
        So inshort we do not know about this yet

  • If a large proportion of disease progression were from previous damage, be it driven by microglial, macrophage or plasma cells. Why does PPMS usually progress faster?

    • Not a neuro – I have a friend in the same situation as you are, and he is very young 25 yo, only started terifluminode treatment. Symptoms mostly muscle weakness related, imbalance starts to get more and more noticeable the longer he’s off steroids, then he goes back to hospital to do another one for peace of 4~6 month, according to him. the peace in between steroids is getting shorter, he doesn’t get real relapses, except the first one.

      Are you on any DMT’s now? Did you ask the question to your neuro?

      This reminds me of SEL prof G categorized,

    • No I dont know, it will be experimental and unproven at the moment as I have not heard there is success.

      • Ok
        So one of my all time passion is cancer research and for time to time ms and cancer cross the same pathFinally, we explored the translational potential of these findings
        by testing whether known myelination-inducing pharmacological
        agents could differentiate GBM cells by increasing endogenous
        SOX10 levels. We first treated cultured G144 cells with two
        compounds: the clinically-approved anti-asthma medication
        Pranlukast and the cell permeable cAMP analogue dibutyril
        cAMP (db-cAMP). In addition to blocking cysteinyl-leukotriene
        1 receptor, Pranlukast inhibits GPR17, a negative regulator of
        oligodendrocyte development38–40. GPR17 is normally expressed
        in immature oligodendrocytes38 and, importantly, was strongly
        induced in G144 cells purified from the CC and upon SOX10
        overexpression (Figs. 1d and 5b). db-cAMP treatment of normal
        progenitors results in elevated intracellular cAMP levels, which
        promote oligodendrocyte differentiation, likely by phenocopying
        GPCR activity41,42. Treatment of G144 with either compound for
        2 weeks was sufficient to increase endogenous SOX10 levels and
        differentiation to O4+ pre-oligodendrocyte cells, leading to a
        reduction in proliferation (Fig. 7a–h). These effects were fully
        dependent on SOX10, as no differentiation was observed in drugtreated
        SOX10 knock-out cells (Supplementary Fig. 7a, b). Next,
        we administered Pranlukast to tumour-bearing mice in vivo. As
        Pranlukast has poor BBB penetration43, we delivered it
        intrathecally using osmotic mini-pumps. Strikingly, we found a
        significant increase in the number of SOX10+ cells in Pranlukasttreated
        tumours, which was accompanied by a dramatic reduction
        in proliferation relative to saline-treated controls (Fig. 7i–l).
        Pranlukast did not affect endogenous inflammatory glia,
        indicative of a direct effect on the tumour cells (Supplementary
        Fig. 7c–e). We conclude that a subset of GBMs can be induced to
        undergo pre-oligodendrocyte differentiation with small molecules
        that raise SOX10 levels and propose that such differentiation
        therapy may be an effective strategy for curtailing tumourigenesis
        and recurrence.

        The white matter is a pro-differentiative niche
        for glioblastoma

        https://pubmed.ncbi.nlm.nih.gov/33846316/

  • Getting my first vaccine-shot in 2 weeks (finally!). I was planning on taking paracetamol before and after, to lessen the side-effects (like I did whilst on rebif). But now the popular press is saying that paracetamol (and NSAIDs) can weaken your immune response to the vaccine. I’m aware of some older studies on prophylactic paracetamol administration at the time of vaccination with children, that do mention reduced anti-body response, but I’m not sure what to make of that for covid-vaccination… Any thoughts?

    • Yes this is very interesting and is something I have believed for some time that the grey matter damage may be due to the inputs from the white matter and this is why when pathologists look in the grey matter they dont see much going on because the the action occurs elsewhere. However, sadly I am not posting on MRI papers at the moment.

  • This message is for Professor Gavin and Professor Julian Gold. I believe this could be another potential way to get funding for the use of antiretrovirals for EBV. The National Institute of Neurological Disorders and Stroke are currently funding this study : HERV-K Suppression Using Antiretroviral Therapy in Volunteers With Amyotrophic Lateral Sclerosis (ALS).

    They are recruiting 200 volunteers. Here is the link as well as another link to clinical trials..gov. It is possible that they could help fund such a trial for multiple sclerosis as well but for EBV.

    Sponsor:
    National Institute of Neurological Disorders and Stroke (NINDS)

    Information provided by (Responsible Party):
    National Institutes of Health Clinical Center (CC) ( National Institute of Neurological Disorders and Stroke (NINDS) )

    Study Type : Interventional (Clinical Trial)
    Estimated Enrollment : 200 participants
    Allocation: N/A
    Intervention Model: Single Group Assignment
    Masking: None (Open Label)
    Primary Purpose: Treatment
    Official Title: HERV-K Suppression Using Antiretroviral Therapy in Volunteers With Amyotrophic Lateral Sclerosis (ALS)
    Actual Study Start Date : April 1, 2019
    Estimated Primary Completion Date : February 1, 2022
    Estimated Study Completion Date : February 1, 2022

    https://clinicaltrials.gov/ct2/show/NCT02437110

    https://www.ninds.nih.gov/Disorders/Clinical-Trials/HERV-K-Suppression-Using-Antiretroviral-Therapy-Volunteers-Amyotrophic

  • Is this the infamous antiretroviral trial in Boston professor Gavin was talking about ?

    Link : https://clinicaltrials.gov/ct2/show/NCT04880577

    Tenofovir Alafenamide for Treatment of Symptoms and Neuroprotection in Relapsing Remitting Multiple Sclerosis

    Sponsor:
    Harvard Medical School

    Collaborator:
    Gilead Sciences

    Information provided by (Responsible Party):
    Michael Levy, Harvard Medical School

    Go to sections
    Brief Summary:

    As the in vivo reservoir of the Epstein-Barr virus, B cells play an important role in the perpetuation of MS disease activity. B cell depletion therapy with medications like ocrelizumab or rituximab have proved very successful in preventing clinical relapses and MRI activity in MS, but incomplete in terms of neuroprotection and symptomatic outcomes. Ocrelizumab and rituximab only target naïve and memory B cells expressing the CD20 marker but do not deplete the wide spectrum of B cell lineages including plasmablasts and plasma cells, which are also key reservoirs for EBV. This is particularly relevant to the mechanism of action of TAF, since EBV lytic reactivation occurs in coordination with B-cell differentiation. In vivo, the initiation of plasma cell differentiation provides the physiological trigger for EBV lytic reactivation, and EBV utilizes the plasma cell differentiation program to replicate. As these cells are ineffectively depleted by anti-CD20 treatment, the use of TAF would be highly complementary as an add-on treatment to anti-CD20 therapy.
    Anti-EBV therapy with TAF in combination with ocrelizumab or rituximab will therefore provide a synergistic approach to cover the whole EBV reservoir.
    The primary aims of the proposed trial are to determine if TAF, at the standard dose of 25 mg/day administered for 12 months:
    i) is safe and well-tolerated by individuals with RRMS over a period of treatment of 12 months; ii) leads to an overall improvement in fatigue, as assessed by the Modified Fatigue Impact Scale by 12 months; and iii) causes a reduction in serum concentrations of neurofilament light chain (NfL), a marker of neuronal damage in MS.

    Study Type : Interventional (Clinical Trial)
    Estimated Enrollment : 60 participants
    Allocation: Randomized
    Intervention Model: Parallel Assignment
    Masking: Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)
    Primary Purpose: Treatment
    Official Title: Tenofovir Alafenamide for Treatment of Symptoms and Neuroprotection in Relapsing Remitting Multiple Sclerosis
    Estimated Study Start Date : May 15, 2021
    Estimated Primary Completion Date : February 14, 2023
    Estimated Study Completion Date : February 14, 2024

  • Can you have a covid-vaccine (pfizer) when you’re having a relaps or a pseudo-relaps?
    Last week, some old (and some new) symptoms started again (maybe related to stress, as I’m being fired). My first shot is next week, and my symptoms do not seem to get better.

    • If this question has been answered somewhere before (I wasn’t able to find it on the blog), I would be very grateful if someone pointed me where to find it…

    • I guess there’s just no evidence on that:
      -who would bother taking a vaccine while having a relaps pre-covid?
      -and now: if you’re taking steroids, no point in having a vaccine – so it’s just the odd pwMS who’s having a ‘mild’ relaps, guess that’s just too small a population

  • I wanted to ask if there is a difference in DMTs and how effective they are individually against brain versus spinal lesions? If so, please could you do a blog article on this? Is there a more effective DMT for spinal lesions? Many thanks.

    • I second that question – I always assumed more effective DMTs are just ‘generally’ more effective against all types of lesions. But if there’s evidence suggesting that some may be more effective against spinal cord lesions specifically…

      • Ocrevus “healed” my cervical spine lesions. Damage is done and scaring remains, but the lesions are no longer enhancing or multiplying. Just my experience. Only had four cycles. Best of luck.

        • my spinal lesions were healed even before I started a DMT – then I got new ones in the following years.

  • Is it possible to develop symptoms due to a DMT?
    I started teriflunomide almost 3 weeks ago. Last week, I started having vision troubles in the left eye, and numbness on the left side of the face.
    I was off medication for 8 months, with no symptoms, and now I start a DMT again (just to be on the safe side) and I’m getting symptoms? Is this something that is known to happen? And if so, is it usually transient?

      • thank you – I also would think it highly unlikely if asked in theory.
        But the timing is just so strange: years without symptoms (even in the 8 months without DMT) and then 1 week after starting teriflunomide, I suddenly develop symptoms…
        If prof G (or a neuro) has some thoughts on this?

        • This happened to me after Ocrevus as well. Supposedly right after treatment you can get “cytokine storm” which causes these types of symptoms. My initial worsening improved but then re-appeared and has persisted for months. I am due second infusion soon – if this happens again with a similar timing I will know it’s due to the drug. But Prof mentioned my reaction is due to pre-existing damage (had MS since 2010 but only started Ocrevus last year as first therapy).

          Cheers,
          CK

  • Prof G has often talked of the benefits of a low-calorie diet. As a PwMS with a borderline unhealthy BMI and a family history of Diabetes, I thought this article was quite exciting
    https://www.theguardian.com/society/2021/may/15/how-to-cure-type-2-diabetes-without-medication

    It talks about Dr Roy Taylor’s research on preventing and reversing Type 2 Diabetes by means of reducing BMI
    “Professor Roy Taylor revolutionised treatment for type 2 diabetes with a groundbreaking study that showed the disease could be reversed through rapid weight loss”

    If this diet helps reverse Diabetes 2 via weight loss, it should help control MS too.
    I would like to hear your comments on the topic

  • I hate to do this,its not my tipe …

    Anyway

    Happy birthday …to me
    Happy birthday …to me
    Happy birthday …to me…..La la la la ……….aaaa

    🙂

    • Thanks for sharing this video Luis. Very powerful. As I continued to watch, I feared Justin was going to die at the end of the segment. I was happy to see his resolve despite the significant challenges he faced. However, I could not help but notice the physical and emotional similarities between MND and MS. So I am left with mixed emotions, yet more motivated than ever to keep fighting and pushing forward.

      • Yes, thank you Luis. One can not watch the video without awe of Justin’s perseverance and love of life, and to feel personally enough bravery to keep pushing one’s self forward. It was a sort of pep talk that I hadn’t realized I was currently needing.

  • B time 🙂

    A while back i came across this paper

    Recirculating Intestinal IgA-Producing Cells Regulate Neuroinflammation via IL-10

    Well the mavens on the blog did not like the idea

    Now Racaniello and is “collective cyborg” explain this paper

    :

    They even talk about atacicept,baff,tacci etc

    • Thanks……It gives insight into the mind of the basic scientist….Sad to say I wonder if a little bit of knowledge is dangerous:-)…some of the baseline knowledge is wrong….(to paraphrase “Mouse models generaly model progressive disease” and it’s induced with Cholera toxin…p.s. it is Whooping cough toxin) should we believe the conclusions or not?, sadly I had slit my wrists before we got to the end of the 70mins….I wonder if we have been in lock-down too long and I wonder what was going through Racaniello’s mind, he is completely silent for most of the time….some reader says “I could listen to their brainstoring all day”…I guess the response could be “Get a life”. :-)…watch from 1:06 …… at least the cat is happy….microbe.tv. taking about MS…I am sure they will have a laugh if I do microbes

      • Lolll

        Thats why i like you 🙂

        You spend the time listen

        Prof: Racaniello has 6 podcasts
        Virology
        paracitism
        Neuroscience
        Immunology
        Evolucion

        (Forgot the last one)

        Most of the times we let the others do the talk (thats is words)

        I also sawl that lack of knowledge about EAE

        They are Immunologists a guest they dont know much about ms mouse models

        • I saw the one “Vincent explains the properties of the SARS-CoV-2 UK variant and why claims that it is more transmissible are not supported by experimental data”. (https://www.youtube.com/watch?v=wC8ObD2W4Rk)….I guess the real data shows his idea should have been shot-down in flames:-)..However the comments were great “Hi Vincent , I don’t know how can I express my appreciation for your time and efforts in educating the public in this critical time . Covid-19 will disappear sooner or later but your efforts will be remembered in the history of science”

          What will I be known for….”Talks alot of BS” .I suspect…:-

  • Should someone with MS take the Sputnik vaccine if given the chance?

    Asking because it is supposed to have a ‘live virus’ (adenovirus)
    I remember reading that people with MS should avoid vaccines that contain a live virus

    https://www.nytimes.com/interactive/2021/health/gamaleya-covid-19-vaccine.html
    “The adenovirus pushes its DNA into the nucleus. The adenovirus is engineered so it can’t make copies of itself, but the gene for the coronavirus spike protein can be read by the cell and copied into a molecule called messenger RNA, or mRNA.”

      • Yep MD2 is correct Astrazeneca is a live adenovirus, but is disabled so it cannot replicate like a live virus could. Sputnik is a combination of two different adenoviruses both carry the spike protein

  • I had Alemtuzumab in 2017 and since then been NEDA. However something strange has happened in my last MRI that’s never happened before. Also before the scan I was on Meraformin and Sarvistin for 8 months. The scan showed a shrinkage in the lessons. Does one swallow make a summer. No. But surely where there’s smoke there’s a fire?

  • I had Interesting discovery yesterday: I found an ophthalmologist that had the “add on” software for optical coherence tomography (OCT) to measure retinal layer thickness. She said that standard OCR avail most places in states doesn’t have add on software as it costs more to doctor. But cost is not passed on to patient, at least in her office. However, the doctor said she would need to look into how to interpret changes to thickness in pwms. We both agreed a baseline as good, but then what? Are there parameters for an ophthalmologist to determine rapid thinning for an individual and does it vary by age, length of disease? Is there a scientific article or resource that could guide an ophthalmologist to interpret active thinning of pwms’s retina on Ocr?

  • Hope ‘Brain Health: Time Matters’ is included/involved Prof G

    Stop Multiple Sclerosis is the theme of this year’s World Brain Day, taking place July 22 to raise global awareness of multiple sclerosis (MS) through seminars, conferences and other presentations.

    “Every year, we use World Brain Day to highlight an area of neurology that needs the world’s attention,” Tissa Wijeratne, MD, the World Brain Day chair, said in a press release. “Every five minutes, someone receives the life-altering diagnosis of multiple sclerosis, so the urgency of this matter could not be more apparent.”

    The event is sponsored by the World Federation of Neurology (WFN) and the MS International Federation (MSIF), which are inviting all those living with MS, caregivers, healthcare providers, and MS organizations to participate in the presentations to use the #WorldBrainDay2021 hashtag. Participants also can use event banners and logos, which are available in the World Brain Day 2021 Toolkit.

    • Wow this is RM10….T cells, T regulatory cells and secondary progressive MS what a trial.

  • T time

    A COVID-fighter’s guide to T cells

    Key points:

    The researchers evaluated all 25 known human T cell response studies conducted between the beginning of the COVID-19 pandemic and March 15, 2021.
    The studies show human T cell responses against 1,434 CD4 and CD8 epitopes. Epitopes are sites on SARS-CoV-2 that T cells can recognize.
    Grouping these studies together for this larger analysis has revealed several “immunodominant” sites on the virus. These sites are where T cells are most prone to homing in on.
    This broad T cell response makes it difficult for SARS-CoV-2 variants to acquire enough mutations to “escape” the body’s response against the virus

    https://medicalxpress.com/news/2021-05-covid-fighter-cells.html

  • A question about UTI’s. If you have a urine sample positive for leukocyte esterase, but no symptoms of infection is it normal not to treat?
    Thanks.

  • Sphingolipids malfuntion

    Scientists discover a new genetic form of ALS in children

    https://medicalxpress.com/news/2021-05-scientists-genetic-als-children.html

    And ppms

    The lipid with the
    most significant differential abundance between the CSF of
    progressive compared to relapsing-remitting patients was
    ceramide C24. Ceramides are sphingolipids whose importance
    in multiple sclerosis (Jana and Pahan, 2010) has beensuggested by a number of old and new reports, including
    the detection of altered levels in post-mortem multiple
    sclerosis brains (Cumings and Goodwin, 1968; Halmer
    et al., 2014) and the more elevated levels in the CSF of
    multiple sclerosis patients compared to non-multiple sclerosis
    controls (Wheeler et al., 2008; Vidaurre et al., 2014).
    The detection of the ceramide species C24 as the lipid with
    the most statistically significant difference in abundance
    between the CSF of progressive and relapsing-remitting
    patients brings up the question of the source of this sphingolipid.

    A metabolic perspective on CSF-mediated
    neurodegeneration in multiple sclerosis

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