#NewsSpeak: ECTRIMS-ACTRIMS 2017

See what will be hot at ECTRIMS 2017! #NewsSpeak #ECTRIMS2017

The rejection and acceptance emails for submitted work to ECTRIMS-ACTRIMS 2017 have now gone out. You can get a flavour of how the field is moving from  the Scientific Programme. Please note our Social Media Session on Thursday. We have managed to get a B-cell vs. T-cell debate, or rumble in Paris, between the heavy weights onto the programme. The debate is being chaired by a card-carrying immunologist who we hope remains impartial. 

42 thoughts on “#NewsSpeak: ECTRIMS-ACTRIMS 2017”

  1. Yawn; same old topics – same old speakers. Looks as if the programme has been put together for the benefit of Pharma. Not much of Barts-MS on the programme.

    1. Anon 2:09: By now you should know how pharma loves this disease. A cash cow, a fiscal perfect storm. The lymphocyte debate? What debate? B and T-cells work in concert. The auto-reactive T-cells recognizing purported "self-antigens" on APCs. B-cells which may act as APCs presenting self-antigens or EBV Ags.

    2. "Meeting for the benefit of Pharma"….Yes it's a trade show where companies show their wares and pay handsomely for that pleasure. It is about educating the working neurologist.Not Much of Barts-MS on the programme…maybe have a closer look. As to platform ProfG is there as usual but talking on something new but I agree these are often reserved for the same old faces, the crowd pullers, in some peoples eyes in other's some are tooth pullers who turn up and give you a Striker conversation Airplane moments, because they are bad speakers.https://www.youtube.com/watch?v=ZqtNxNRCcGgcheck out 0.38-1.32 🙂

  2. 15 years after my diagnosis I still stupidly hope that some major breakthrough will be announced. These conferences (ACTRIMS, ECTRIMS, AAN, MS Frontiers, European Charcot Foundation etc. etc.) are a nice trip out to lovely locations such as Paris, Madrid, Vienna… The same names appear each year doing the same old presentations. Will the cause of MS be announced? Will a timetable for getting neuroprotective and neurorestorative treatments be annonced? I doubt it, but the same old MSologists get a gala dinner, neuro-bowl, and an opportunity to take their partners along for a nice week away paid for by academic institutions or pharma. In the sge of austerity and overworked neuros, you'd think these events would be scrapped and more use made of video conferencing. Please, please announce something big this year!

    1. Ahh those were the days. Times have changed, these meeting are purely academic, no freebies, no spouses, no entertainment, just hard graft. We call it austerity ECTRIMS.

    2. It must be dreadful being an MSologist. This is from the Ectrims 2017 website:Aside from neurology and neurosciences, Paris is well known for fashion, culture, food and entertainment. It benefits from a very convenient metro and bus public transportation system, but do not hesitate to rent the Velib bikes to discover the whole city, enjoy the banks of the Seine and all the Parisian jewels. Also take time to have a drink in the many Parisian cafés.

    3. "Please, please announce something big this year!"I suppose it might take another year (cheapo Berlin then:-), but may be OCTRIMS (online committee for treatment and research in MS) is not too far away. Focusing research in the right place to (i) treat more pwMS better *now* and (ii) set the stage for add-on therapies may ultimately downsize these meetings, but will this be better for pwMS?

    4. Dr KS, sorry for the diversion and thanks again for that Oppenheimer paper, but I'm afraid you never told me your opinion about the profound correlation of lateral spinal lesions with denticulate ligaments, as described in that paper. How can this be?

    5. Perhaps it's the "soluble factor" in the CSF Otto Marburg hypothesized in 1906. His book is available online and for free; how's your German: https://archive.org/stream/diesogenannteak00marbgoog#page/n11/mode/2upElse here is a review by Hans Lassmann that refers to Marburg: http://ac.els-cdn.com/S0014488613003610/1-s2.0-S0014488613003610-main.pdf?_tid=e8c1f276-7709-11e7-9c63-00000aacb35f&acdnat=1501627191_0c0762d79f741ddf7f6bdb6764f4d863

    6. Sorry, it makes no sense. Denticulate ligaments are solid collagen fibers. They are firm strings that penetrate the spine. What soluble factors have to do with a structure like this?

    7. I get the sense you want me to say it is to do with trauma/force, but I don't think there is any evidence. There's plenty of demyelination in the cord all over, and more in the grey than the white matter, so I think you need to look elsewhere.

    8. No soluble factor with demyelinating capabilities has been found, either. None since 1906. In what way would a trauma induced lesion look different? I mean, what are the evidence that would convince you?

    9. Denticulate ligaments are thicker-stronger, go deeper inside the spine, and have more micro-anchoring points in the cervical region, less in thoracic and even less in lumbar region. Two different anatomical studies in 2012 and 2014 confirm this. https://www.ncbi.nlm.nih.gov/pubmed/22555553https://www.ncbi.nlm.nih.gov/pubmed/2389754550% of MS lesions are in the cervical region, less in thoracic and some in lumbar region. Combined with the Oppenheimer study, isn't this enough evidence?I ask for a comment on a correlation that has never been refuted since the single Oppenheimer study and i get a link about how toxic are RRMS B-cells "to rat and human neurons" in vitro! How does this explain the correlation of lateral spinal lesions with denticulate ligaments?!Come on, why don't you admit that this is an understudied part of MS and that you simply don't have an aswer yet. In fact, your team could do such a study. Why don't you give it a try?

    10. No Dr KS, you have looked at something else.I am talking about MS lesions, but you studied the print that lesions leave behind, namely demyelination and axonal loss.Lesions are dynamic entities, they come and go during a life with MS.They are a measure of hits against CNS, they represent the number of different blows in the timeline of MS.Most patients-readers of this blog will agree that all those years with MS, their MRIs show more cervical lesions than thoracic and lumbar. Several studies support this finding:https://www.ncbi.nlm.nih.gov/pubmed/14745058http://www.nature.com/sc/journal/v53/n7/full/sc2014238a.htmlSo, it is widely acknowledged that cervical region is more frequently involved as far as lesions are concerned.Now, your paper tells us nothing about the number of lesions and it couldn't do otherwise, since it is an anatomical study AFTER a whole life with MS. What you measured was the ACCUMULATED BURDEN of all lesions/hits that were inflicted to CNS during the whole MS timeline, in terms of demyelination and axonal damage.Interestingly, you found that this accumulated burden was generally the same for all levels of the spinal cord, and this is totally convincing.So, we are presented with two facts that seem to contradict each other:a) Spinal lesions are more frequent in the cervical regionb) Demyelination and axonal density loss is the same for all levels of the spinal cordHow can this be? The answer is straightforward:Spinal lesions don't appear in random, but have a predilection to appear in certain places. That way, repetitive lesions on the same spot tend to overlap, leaving their print on top of a previously inflicted print, demyelinating an already demyelinated region, damaging an already damaged axon. So, after a lifetime with MS there are equally visible marks in all levels of the spine, on and around those predefined hot spots.That way propositions (a) and (b) are both true. The hot spots for spinal lesion development are the anchoring points of the denticulate ligaments.Your study does not disprove Oppenheimer, but supports his views.

    11. MD2, I have told you before that according to the theory that i have successfully applied to myself, there is a different process for brain and spinal lesions. They share a common body problem, but the sequence of events that leads to damage is totally different:Spinal lesions are caused by swift vertical movements of the spinal cord inside the vertebral column that stretch the denticulate ligaments and damage the soft CNS tissue they are anchored to.Brain lesions are caused by spontaneous, swift, reversed blood flow that, unable as it is to escape the closed compartment of the skull, exerts its force on the weakest venous path available at the time.

  3. Who presents the talk on progressive MS? It must be crickets. How can a neurologist advise a fellow neurologist on treating progressive MS when there is no approved treatments, except ocrezulimab based on a paltry response in a small selection biased subtype of inflammatory PPMS patients which is available only in the USA and not available to SPMS patients based on imaginary pharma based subtypes of MS?All these years and no treatment of progressive MS. ~20 treatments for the inflammation phase of RRMS generating 20+ billion per year in profits, including large sums going to the recurrent presenters and moderators at the above conference, which hopefully soon will become public knowledge in all countries.There are no current approved treatments of neurodegeneration, remyelination and neurorestoration. Do any current treatments actually improve a MS patient's EDSS or clinical condition or just prolong them from going down the drain? The only one that has shown this positive effect that I could find is mesenchymal stem cells in early trials by Dr. D. Karussis and Dr. P. Connick. I do look forward to the glial cell presentations in progressive MS, as both T and B-cell therapies have not panned out in progressive patients.If EBV is thought to cause MS by many, which has been known epidemiologically for years, why is an urgent trial for this not already done for this via a vaccine to prevent this horrible disease for future generations? Why has the MS world not thrown it's weight behind Dr. Pender's work on primed CD8 cells against EBV driven B-cells in follicles in the brain if EBV is driving MS?

    1. "There are no current approved treatments of neurodegeneration"Ectrims 2016https://www.ectrims.eu/wp-content/uploads/2016/09/ECTRIMS-Highlights-Release-Day-3-lipoic-acid-shows-great-potential.pdf"The rate of brain volume decline over time in those who took lipoic acid supplements was 0.22% per year and 0.65% per year in those who took the placebo. This is a 66% reduction, which is statically significant (p=0.004)"

    2. Thanks Luis and these results are great if they can be replicated in larger phase III trials, which are not completed. There is currently no approved drug for neurorestoration, neurodegeneration and remyelination. It would not be in pharma's best interest to support a nutraceutical like this as it would mean less money for them despite lipoic acid's robust 66% reduction in atrophy. One would think the research world would be behind a discovery like this.

  4. The funniest thing is that the most effective treatment for MS was never even developed for MS and is relying on charities to push it through clinical trials: cyclophosphamide.

    1. Problems include being too cheap, but also adverse effects. Another drug C much more promising:-)

    2. Cladribine is not more promising than cyclophosphamide. Not even close. Yes, it has far less side effects, but at the cost of vastly inferior efficacy. Just look at the cladribine studies vs the HSCT ones. Vast difference.It's weird. Cyclophosphamide as approved in the US in 1959. Yet it is the best drug to treat MS by a large margin. All the 'advances' in MS over the last 20-30 years haven't been advances at all. We have yet to invent a chemical better than one they invented in 1959.

    3. Cyclophosphamide isn't a sledgehammer, total body irradiation is a sledgehammer.Both are better than MS.

    4. "Both are better than MS."No, not necessarily. That is simplistic, blinkered thinking. It depends on the nature of a particular person's MS. And not everyone tolerates drugs, therapies the same.

    5. MouseDoctor2Wednesday, August 02, 2017 11:09:00 amIf all you have is a (sledge)hammer, every problem looks like a nail.Do you have Ms?

    6. No I don't, I've been researching into MS for 30 years and I have a family member who does have MS, also two previous colleagues of mine developed MS.The point I was making is that we need more selective methods of treating MS other than a general clobbering of the entire immune system with agents like cyclophosphamide. Selective anti-B cell agents for example.

    7. Cyclophosphamide may be the answer for ms and very successful in treating all forms of ms but the side effects are worse than the disease and are devastating including malignancy. I would have to agree with MD2 as it is too dangerous. Don't believe me read its side effect profile on any website.

    8. We all appreciate what you do MD. The problem is B cells are not the whole story. They are a major part of the story and I commend you for your work in that area but the innate immune system as well as T cells have been implicated in MS.

    9. " I would have to agree with MD2 as it is too dangerous""It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system"

    10. T cells have been implicated, but where is the evidence that they are essential? Where are examples where T cell-specific therapies have had major impact?T cells respond to myelin basic protein….So what.Yes I am being devils advocate

    11. "I bet that if you had ms you would consider (sledge)hammer approach".I refer you to Prof G's post on cyclophosphamide today.

    12. T cells are not the main game. Nor is the innate immune system. B cells, particularly memory B cells are, as I have learned from this blog. But they do play a part. MS is a terrible, terrible disease, and no part of the disease should be left in place to take its toll on patients.

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