Google Hangout at ECTRIMS2017

   Ello Ello my little British Chums

Soon we will be swapping the “Stiff upper lip” for the “Land of  Joie de Vivre” as ECTRIMS moves across “La Manche” and ACTRIMS moves across “the Pond” to Paris 2017.

NGD will be swapping the G&T, for a glass of Pastis and Champers

Only Joking……….she’ll give me a thump for saying that…..

However we will be back doing a Google Hangout Live to bring you meeting highlights and answering your questions.

So why not have a browse through the programme and tell us what you want to look at.

Send an email or write it below,

Ectrims actrims from BartsMSBlog

I’ve had a quick look through and know some of the places I’ll be making a bee line to…..I can’t wait to find out more about “Copaxone despot”…..I mean glatiramer acetate depot. 

No sooner than you can say that using 40mg thrice a weeks is maybe not that inventive/novel compared to daily doses of glatiramer acetate  20mg dose we are now seeing “80mg depot”. Not once a week, as I predicted…..but once a month.

Will it work and if it does what does it say about daily injecting.

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  • Copaxone once a month. Now that makes it more appealing to me.

    Page 33, Fresh fish consumption independent of vit D levels and lower rate of MS. This sounds interesting.

    Does this tell us anything about the cause of MS?

    • On second thoughts could Copaxone once a month lead to worse or more intense psychological problems (i.e depression) as it's a higher dose?

  • Great to see Goole appearing on the neuroresearch map at last – though wouldn't it be better if you did this from Paris?

  • Lol MD, your first mistake was assuming that I didn't look at the other posts, second was preemptively mentioning the thump.

    Jokes aside I'm at amiss on what is useful in the programme. Horizons in progressive MS seems interesting. I think I'll be spending my time at the posters this year!

    • There is loads of stuff.

      Maybe our paper on autoimmunity and neutralizing antibody stuff after have raised some eyebrows and we will see some citations to get my H factor up.

      "Leukocyte repopulation following alemtuzumab treatment in relapsing-remitting MS contains multiple regulatory immune cell types
      W. Gilmore (Los Angeles, US)"

      This will no doubt ctry counter the suggestion that we made that the B cell repopulation in the "relative" absence of T cell regulation (CD4 & CD8) was part of the problem of autoimmunity.

      Is this a Genzyme poster or are we being ganged up against?:-)

      Then there is "Preferential reconstitution of regulatory B cell subsets following alemtuzumab treatment in multiple sclerosis
      Y. Kim (Goyang-si, KR)

      Is this the reason memory B cells went down, because regulatory B cells were going up? Did we miss something if you look at percentages on flow cytometry if one subset goes up the other must goes down.

      But if there is so much regulation around…..why do 50% of people get secondary autoimmunities and over 80% get anti-drug antibodies after alemtuzumab. Maybe are spending too much time of working why alemtuzumab works to stop MS…it's the memory B cells:-)

      Maybe it will be explained in "Efficacy of a third course of alemtuzumab in patients who experienced disease activity after the initial two courses: pooled analysis of CARE-MS I and II A. Traboulsee (Vancouver, CA)".

      Will they come clean and acknowledge that neutralizing antibodies occur and show the individual responses before and after the third infusion as opposed to the group means (Of course they won't do that will they)…because we already know the third infusion can work but that this is where the neutralizing antibody response time bomb starts ticking will be ignored but there are many more people with pre-existing antibodies before the infusion and if we saw individual responses we could see the scale of the problem that we and others know can potentially occur.

      Abrogation of the lymphocyte depleting action of Alemtuzumab by neutralizing antibodies – a case report C. Eggers (Linz, AT)

      So the £21,000 stops working in some people treated. The question is how many? Genzyme have the data they have done the phenotyping as the evidence was presented……will they show it.

      What else are we going to pull out of the hat?

      A central role of B cells in MS control and causing autoimmunity after alemtuzumab D. Baker (London, UK)

      There there the data we all want to know

      Alemtuzumab-treated patients with relapsing-remitting MS show low rates of conversion to secondary progressive MS: 6-year follow-up of CARE-MS I and II D. Horakova (Prague, CZ)

      Prof Coles will pick the clinical highlights what will he pick?

    • Lipoic acid in secondary progressive MS
      Conclusions: LA demonstrated a 68% reduction in annualized PCBV and suggested a clinical
      benefit in SPMS while maintaining favorable safety, tolerability, and compliance over 2 years.

      Classification of evidence: This study provides Class I evidence that for patients with SPMS, LA
      reduces the rate of brain atrophy. Neurol Neuroimmunol Neuroinflamm 2017;4:e374; doi: 10.1212/

      This was presented last year at Ectrims but no one care

    • Doubt it will be close to the "68% reduction in the rate of brain atrophy in LA vs placebo" for 1200mg daily of R-lipoic acid. Even Ocrevus was only 17.5% in BV loss.

      "The reduction in the brain atrophy rate compares favorably with a large phase 3 trial of ocrelizumab (n = 731), reporting a 17.5% reduction in the whole-brain atrophy rate over 120 weeks."

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