Hello everybody at team G. I came across this link on a MS-community forum on the Internet: http://www.japantimes.co.jp/news/2014/02/25/national/potential-cure-for-multiple-sclerosis-to-be-tested/#.UxBbQdtyQQ8 (Potential cure for multiple sclerosis to be tested). I'm no scientist, but usually I'm web-savvy enough to 'debunk miracle-claims'. But I failed this time. Of course if it is ongoing legit research you'll have to wait an see about this ass well, but do you know or see anything more in this then I can? This is as far as my "research" got me. http://www.pnas.org/content/by/yearhttp://www.ncbi.nlm.nih.gov/pmc/?term=Takashi+Yamamurabest regards
I have not found anything on pnas yet but it will surface ina day or two
Looking forward to further news. Takashi Yamamura looks legit:http://www.ncnp.go.jp/nin/guide/r_men/yamamura-e.html
From Berts link:"The National Center of Neurology and Psychiatry has developed a drug that it says might provide a cure to multiple sclerosis.The center announced Monday that it will start a three-month clinical trial from March on nine patients. If the drug’s efficacy is confirmed, it will move on to a large-scale trial."It seems they are moving fast. Japan must have a more efficient drug development strategy. I wonder if a pharmaceutical company is involved or if this is being done soley by this national institute.
We need more info before comment. Probably irresponsible reporting but let's see
Prof G and Mouse, you guys mention that you believe that PPMS and SPMS are the same disease (based on natural progression timescales and age of onset) and are trying to push through acceptance of the same in the general community. Why then don't any of your trials for SPMS include those with PPMS? As a newly diagnosed PPMSer I am losing all hope in the future at all. I can't even see trials commencing in the near future for us PPMSers because it seems every time you see the term "progressive" MS thrown around it is referring specifically to SPMS. At present is there absolutely anything that can be done for PPMS in the UK??I know Ocrelizumab is in trials as is fingolimod (can't seem to find any patient experiences in forums) even still it may be along way off before we can start treatment.. and who knows what EDSS we'll be at then.. Are there any possible ways you can be treated off label?? Or is it simply the case that we are left to rot?? My apologies for the phrasing but that is genuinely how desperately hopeless this situation feels.
The closest phase III trial in progressive MS to reporting, is should end this year in PPMS. If this is positive it is a game changer. First thing I would ask is to determine whether you are a gadolium-enhancing PPMSer, because you could respond to some treatments and I believe that ProfG has a number of PPMSers on these options off label.The reason people do trials in SPMS is that it is easier to recruit to do trials because there are more SPMSers and when you do trials if there are large differences between the participants means that the trials need to be large and this means there is more cost.In the trials ongoing at QMUL there are a range of disease from the onset of first signs onwards
Are the treatments for gadolinium-enhancing PPMSers suitable for gadolinium-enhancing SPMSers (if such a person exists)? I am not familiar with the technology so don't know whether the Gd enhancing aspect is relevant to SPMSers as well. Thanks
Yes there is no difference in my EAE, it was hown with one of the beta intereferons that relapsing SPMSers did better on drug than non-relapsing (Gd enhancing) SPMS
Thanks for that
Recently a post on the beneficial effect of sequestration of t-cells into the intestine on EAE was posted. Once blocked by alpha4beta7 Ab the increased availability in the periphery might increase EAE. T-cells could still migrate into the CNS and trigger EAE since the blocking Ab was specific for alpha4beta7 and did not block alpha4beta1. Author reply follows.RE: blocking alpha4beta7 with natalizumabGKrishnamoorthy replied to sswiatlo on 26 Feb 2014 at 09:26 GMTOur data does not contradict the proposed mechanism of Natalizumab. We agree with the reader’s comment that blocking the alpha4 integrin would still be sufficient to prevent EAE, as it would indiscriminately target the migration of T cells to the intestine as well as into the brain. In our study, we used an alpha4/beta7 blocking antibody to target T cell migration to the intestine but not to the brain. Please note that alpha4/beta7 is not required for migration of T cells to the brain (Döring, A et al 2011 Eur J Immunol). Previous reports also showed that Th17 cells do not use alpha4 integrin for the migration to the brain (Rothhammer, V. et al 2011, J Exp Med & Glatigny, S. 2011 J Immunol). In sum, we conclude that in certain genetic backgrounds blocking intestinal homing of T cells might increase EAE by enhancing the availability of myelin-specific T cells.No competing interests declared.
Since the gut is heavily populated with lymphoid tissue, the connection with homeostasis of immune tolerance is implicated. The recent study of C. perfringens toxin and MS and the fact that the lumen of the intestinal tract is directly connected to the environment makes for an interesting hypothesis.
Professor,I hear of a anutoimmune antibody receptor problem. People Making antibodies that have no receptors. They are being treated with IVIG therapy drug is called Flemmogamma. Can this slow down MS?
Just read in Sci Am about exosomes repairing myelin.http://www.scientificamerican.com/article/naturally-occurring-packets-show-promise-for-protecting-brains-nerve-fibers/Same article appears in the print edition. Unfortunately, the papers "cited" are behind paywalls.
There is a lot of information about the prevalence and incidence of MS in Europe, and you have included a links to some articles on the topic, but are you able to say what the definitive figures are for these?Thanks
Team G,I've attended the research days and follow the blog. Lots of articles, lots of noise, lots of discussion e.g big pharma alternative / future of the NHS. I'm assuming your remit includes improving the understanding of this disease and identifying treatments where there are currently none e.g. Repair of damage and stopping progression. How are you doing on these aspects of MS research?
If you have been to these meetings you have seen where our research focus has been. We can not do everything. You can see that we have not had a major visible push in repair but we have been supporting our colleagues elsewhere in Cambridge and Edinburgh who have a major interest in repair. I am aware that a trial has been developed from the Cambridge/Edinburgh connection and then in the USA there are other studies that are recruiting in relation to repair. These are related to academic led studies but pharma is already there and ProfG is involved with some repair trials. We have intiated a number of studies and trials on progression and a re part of a number of pharma studies on progression. We have entered a new era of focus on progresssion and repair which will grow and grow. Unfortunately it will take to long to get these available to everyone but the tide has changed and some of these will come through. If the process can be changed it will be sooner rather than later if the process can not be changed it will be the snail speed that you know.
Mouse, Many thanks for your response. I think the tide is turning and the dots are being joined up. As ever, when you have this disease the new treatments can't come quick enough.
Any comments on the work reported here? www.webmd. com /multiple-sclerosis /news/20140120/ vitamin-d-may-slow-multiple-sclerosis-study-suggests The headline "Vitamin D May Slow Multiple Sclerosis: Study" says it all, however I find the comments in the article rather too negative.""No one knows what the connection between MS and vitamin D is," said Nicholas LaRocca, vice president for health care delivery and policy research at the National Multiple Sclerosis Society. "What they suspect is that vitamin D has some effect on the immune system." Also, what dose of the vitamin might be appropriate isn't clear, he said. "We don't know what a good level would be. There is no scientific consensus on a treatment protocol. We may get to that point eventually," LaRocca said." Exactly how much evidence does he want that extra vitamin d (5000IU a day) is not harmful and may do some good.
we reported on this study on 28 January 2014http://multiple-sclerosis-research.blogspot.co.uk/2014/01/clinic-speak-vitamin-d-levels-as.html
From MSnewschannel website:"A New End Point for a New Era in Multiple Sclerosis Clinical Research?"Since the introduction of interferon beta-1b in 1993, the number of disease-modifying therapies for multiple sclerosis (MS) has grown at a remarkable pace. Currently there are 10 treatments approved by the US Food and Drug Administration, each with varying effects on important clinical and radiographic markers of disease activity.Multiple sclerosis is one of many immune-mediated diseases in which significant advancements in disease modification have been made. Tumor necrosis factor inhibitors have revolutionized the treatment of rheumatologic diseases such as Crohn disease, psoriasis, and rheumatoid arthritis (RA). This therapeutic class has made sustained disease remission achievable in these rheumatologic diseases.Read more »There's a link to a JAMA article (March 2014) about DAF
Anti-TNF therapy has resulted in some RA patients developing MS so we have to be careful about what might appear to be one size fits all therapies.
Lots in the news about statins and Dr Chattaway.http://www.bbc.co.uk/news/health-26630025Why don't Team G ever hit the headlines?
I suggest that you read more widely as you are clearly missing stuff.Then i suggest that you go backto reading where the science originaed and then youwil find a name john greenwood and not Jeremy chattaway. When you do your homw work and find that then you will find team g.However i am glad this phase ii is promising but i ask now what. No phase iii trial has been announced. But to get statins to msers what is the process that allows this to happen. Does it have to be two phase iii as anyother drug would have ro fo then they need eegulatoey apprval who is going to do this for a drug costng a few pounds. When neuros embark on these phase ii do they have the vision of how we getdrugs to msers should the trials work. If the pathway is not clearly mapped out should the study be started. A few days ago it was suggested that there would be a fast track once drugs arw safe in the manufactururer pazys for it. But study was not dne bya manufacturer. This shoud be a test example of prescription whilst evidence for licencing is achieveed.
Was this the new scheme the govt. is introducing to fast track new innovative medicines to patients with life-threatening diseases that was talked about in the Telegraph on 14th March?They say it will get drugs to patients 10 years earlier than it would otherwise. Will it cover MS?
Dear Team G, are you aware of any research on kind OCBs found in MS and prognosis ? All I can find is that OCB negative MSers tend to take benign course and CISers are more likely not to convert. I have recently diagnosed with CIS with MRI suggesting of MS (even got Dawson's fingers), but my spinal tap revealed mirror pattern OCBs (type 4, equal in CSF and serum). This puts a lot of confusion in my diagnosis since that, as most MS specialists, I referred to, says it's unlikely to have MS and such a tap. But I believe, unfortunately, that this is MS :(. So, is any prognostic value of this test?
Sleep loss news:Using a mouse model of chronic sleep loss, Sigrid Veasey, MD , associate professor of Medicine and a member of the Center for Sleep and Circadian Neurobiology at the Perelman School of Medicine and collaborators from Peking University, have determined that extended wakefulness is linked to injury to, and loss of, neurons that are essential for alertness and optimal cognition, the locus coeruleus (LC) neurons."This is the first report that sleep loss can actually result in a loss of neurons," Veasey notes.The Veasey lab found that in response to short-term sleep loss, LC neurons upregulate the sirtuin type 3 (SirT3) protein, which is important for mitochondrial energy production and redox responses, and protect the neurons from metabolic injury. SirT3 is essential across short-term sleep loss to maintain metabolic homeostasis, but in extended wakefulness, the SirT3 response is missing.So, we MSers really need to do something about our sleep loss!
Any thoughts on testosterone and neuroprotection?http://www.sciencedirect.com/science/article/pii/S221315821400031X
http://multiplesclerosis.elsevierresource.com/en/article/S0306-9877(13)00599-9/pdf/intrathecal-immune-reset-in-multiple-sclerosis-exploring-a-new-conceptPublished last year, a bit technical, but the author makes case for intrathecal administration of mab immunosuppressive regimen for treating progressive disease. Hopefully, there will be positive data from rituximab intrathecal study.
Prof G/Mouse, Could either of you guys please explain how you believe EBV acts in relation to PPMS vs RRMS?
ProfG is best placed to do this as EBV is his baby I suspect its role has been or is the same in PPMS and RRMS,but it depends on what your view of PPMS and RRMS is. maybe we can have some guest posts for people with different views on this
Great website-i have found it to be a great way to keep myself informed about MS.I really am tired of the websites that focus on CCSVI and more tired of the Neurologists who are a bit defensive about not being able to treat PPMS. Sometimes,the hardest thing to hear is that you cannot be helped. But It does help to see the more human side of the researchers in this field as well as the Neurologists who do want to help. It gives me hope anyway. SO FIND SOMETHING FAST:-)
Just been on the MS-Smart website. So frustrated to find they are looking at SPMS patients only.Why does is there such a negative attitude towards PPMSer's?Why could they not include some people with PPMS? Don't they need treatment too?
Synthon announces successful outcome of the Phase III GATE study with its generic glatiramer acetate. Synthon today announced that the company’s glatiramer acetate met the main endpoint of a late-stage study in patients with relapsing remitting multiple sclerosis (RRMS). The Phase III Glatiramer Acetate clinical trial To assess Equivalence with Copaxone®* (GATE) is to-date the only Phase III study conducted with a generic version of Copaxone® and has demonstrated an equivalent efficacy and safety profile for Synthon’s glatiramer acetate compared to Copaxone®. http://www.synthon.com/Corporate/News/PressReleases
http://seekingalpha.com/article/2105633-biogen-idec-7-different-insiders-have-sold-shares-this-monthInsiders of Biogen IDEC allegedly are getting rid of Biogen stock Caroline Dorsa (Director divests 20.2%), George Scangos (CEO divests 42.7%) what do they know?
Time will tell
Do you know anything about this antiJCV drug?IkT-001 Pro, would be really nice if it worked.//Swedush Sara
IkT-001Pro, a host-directed tyrosine kinase inhibitor in an extended release formulation, which the company claim clear JC polyomavirus (JCV) infection in at least some patients and is active against the form of the virus that infects the majority of human beings. They claim phase III by 2017.They are in early development stages
Thank´s. I read that they started phase II in 2011 so it´s a slow progress.//Swedish Sara
Enhanced uptake of multiple sclerosis-derived myelin by THP-1 macrophages and primary human microgliahttp://www.jneuroinflammation.com/content/11/1/64/abstractDoes it say that demyelination in MS is possible due to a primary myelin defect?
Maybe but maybe not
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