Attack the Sonic Hedgehog pathway could help the maturation of oligodendrocytes and remyelinate lesions caused by MS? Even old injuries? http://www.eurekalert.org/pub_releases/2015-09/nlmc-ecd092815.php
Post done launched soon
Did you guys see Johanna's post from 9/25!? If this is true, it could remove the biggest barrier for Tysabri use in MS patients worldwide! (Re-posting now, for reference):"Is this realy true? Did they find a cure for PML? Please let it be true,,,http://www.neuroscientistnews.com/research-news/vaccination-horizon-severe-viral-infection-brain"
It is potentially good news for those who haven't been infected with the JC virus but not really for those who already have been infected (which is most of us). Don't mean to be a wet blanket! What we need is an anti viral agent that can clear the virus in those carrying it so the PML problem can be eradicated.
Sorry if I didn't get it but this "the international groups were able to demonstrate that the antibody response was so strong that the patient was soon able to eliminate the JC virus" does not mean that infected people are eligible as well ?By the way, I keep reading some soooo good news these times.Can't wait the ECTRIMS next week ^^
The question is, is the virus cleared from the brain, where it hides behind the blood/brain barrier which antibodies are excluded from? I'm not so sure it is.
BTW the team will be at ECTRIMS next week (or some anyway, not me) so keep visiting for updates.
Do you know anything more about ITK001Pro for a JCV anti viral?
I also read that this publication on the possible vaccine against JCV ... But somehow agree with MD2, they need to demonstrate that JCV was eliminated completely ... Still sounds like good news ... http://multiplesclerosisnewstoday.com/2015/09/25/possible-jc-virus-vaccination-offers-important-implications-ms-treatment/
@ Christian Voltage: MD2 (and all the other MDs over there) are pretty busy - I'm betting he read the end of the URL, and thought it was only talking about a regular vaccine, and didn't have the time to read the full article. I think it's good news for everyone with MS - here's a quote from the article:"The researchers now reveal potential ways to vaccinate against PML preventatively or, if the brain has already been infected, treat it with virus-specific human antibodies."Pretty sure that means everyone (MD2 if I've contradicted you, please feel free to set me straight. I'm no scientist, I'm not doctor, and I'm certainly no mouse). :)
The post has been in ProfG's in box but he's been too busy to comment on the two papers, we'll do it soon.
It is certainly interesting and suggests a vaccine could be near. Will Biogen take up the vaccine and do study to see how much PML occurs.Will Novartis make the ant-JC Virus antibody to help you transition to fingo.Will people move away from at CD49d to ant-CD20.
Thank you anonymus 8:19 :-)
Should the UK become a republic?
Why is there no other word for Thesaurus?
It's a mad, mad world!
Please do a post about 'Burnt out MS'Prof G mentioned it once herehttp://multiple-sclerosis-research.blogspot.com/2012/08/what-do-you-expect-from-effective-dmt.html?showComment=1346225546580#c4181713424096806710
It happens often - for a few days at a stretch, at least once every month - that I feel ill and feverish, but body temperature is either normal or below normal.I feel fine/better after having paracetamol Can this be because of MS?
Now there is a successful trial for ppms, namely the one targeting B cellsWould this make you guys take a different view on hsct or why it works in some people and not others?Could there be an external factor that's driving the reactivation of the disease?
Let us see the data, its out in a week on saturday.I suspect the PPMS trial was loaded with people that may respond in a way we expected. I understand we have been attempting to treat them with rituximab.But the thing about HSCT that I have awoken to is that its safety is much better than it used to be.
Agree with MD on this, I am optimistic but need to see the full results. Maybe Roche should even start a second Phase III looking at irreversible disability instead of simply time to onset of sustained disability at 3 months. So we don't have to wander about the relevance of a 0.5 verses 1 point increase on the EDSS score!
Lemtrada on Monday. Super stoked, hope I'm still young and fit enough to get long-term benefit.
Good luck and I hope it provides the benefit to ou that I really believe this drug can deliver.
Thanks. Would have been best if FDA had approved it prior to needing a scooter to go out, but fingers crossed that its in time for everything else.
Disability Progression starting one year after recovery from CIS. Basically I am told that I must have had inflammation from CIS which caused initail symptoms. This died down releaving the symtpoms but they the underlying nerves had been damaged and have very slowly started to degenerate. Could the neuroprotective part of the new PPMS drug help me. I basically have a lesion on spinal cord but tested negative for MS on a LP.
Transverse myelitis can leave residual disability and does because a larger quantity of axons are involved as they are tightly packed through the spinal cord and also because the long tracts in the spinal cord have poor regenerative capacity, compared to the brain where this is better. If you mean Ocrelizumab this is anticipated to be licensed for RRMS, the PPMS study is ongoing but to qualify you need to meet the PPMS criteria of steady accumulation of disability. As you've pointed out your diagnosis is CIS with a single episode...these are semantics I realise but inclusion into trials and eventual licensing of drugs are quite specific. There are cases of transverse myelitis which never develop MS.
I always wonder why doctors don't apply methylprednisoloninjection close to the spinal cord like they do for neckhernia in case of MS in the spinal cord.
Team G i've been thinking about dental hygiene and MS there doesn't seem much research on it. Having just got home from a check up I told the dentist infections can trigger relapses and also make MS symptoms worse. He said in our mouths we are often fighting low grade infections from bacteria. So we discussed that it would be important for MSers to maintain good dental health so we can fight infections well in other parts of our bodies.
It certainly can't hurt to keep your teeth in good health.
When MSers take Tecfidera and they have a lower lymphocyte count is this due to a side effect of the drug? Or is it that having lower lymphocytes help control the MS? thanks
It is due to the effect of the drug, some seem to be more sensitive than others. Lower lymphocyte levels will certainly have an effect on MS as shown by lymphocyte depleting agents such as Lemtrada. How Tecfidera works is still pooorly understood, which means the fact it's made it to market is surprising IMO.
Thanks. My lymphocytes now are nearly double compared to what they were two years ago when I was very unwell. Tec is my first DMT been on it for nine months. The level has gone up not down so don't know what to make of it. Having another blood test in a few weeks time.
This just came up on the wire:http://www.cnbc.com/2015/10/08/roche-drug-shows-promise-for-multiple-sclerosis.html
Thanks we know, profG will do a post when he has time but is currently doing a 12h plus day with his ECTRIMS duties.So the results of the RRMS trial puts it in the realm of alemtuzumab, but without the side effects and for PPMS there is the dreaded 20-25% level of efficacy. So the question is , is this related to Gadoliunium or T2 lessions. The answer will be of course it is but they may spin an I don't know so that they can get a licence for all of MS not just a subset of progressive MS. If it is really different ?I would say great .....but that says the studies with HSCT and rituximab are made up rubbish. You can't have it both ways
Is the 20-25% efficacy for PPMS unlikely to impress neuros and NICE? Is it even worth having if your walking is so shaky you need a scooter/wheelchair for long trips? You know,getting about in town etc
My walking with PPMS is certainly shaky, but if it was 25% better, I would be able to do a whole lot more. If I had 25% more energy and strength. Or 25% less pain. Don't knock it.
Mous doctor - can you be more specific when you talk about the 10/20 year Alemtuzumab data in the below ECTRIMS hangout you posted? You said that people treated early seems to be 'doing well' but for SPMS they still progressed? Who was doing well? Also are you saying those who took Alemtuzumab who converted to SPMS were progressing or those who had SPMS then took Alemtuzumab were progressing? We're the 20 year cohort NEDA? https://youtu.be/Bbc6aKbyyOQ
I don't know the number of the presentation the people with RR MS were doing better than worsening whereas people starting on almtuzumab after development of SPMS did worse
Could a proportion (even small amount) of people diagnosed with MS actually have Lyme disease?? I ask this as new cases of lyme disease have quadrupled in 12 years in the UK. 60-80% get the bulls eye rash.
A couple of weeks ago there was stories in the news about a study that linked Melatonin levels with MS disease activity-- one article said with a higher correlation than vitamin D. Could you create a post with your opinion on that study when you have some time? Thanks!
http://multiple-sclerosis-research.blogspot.com/2015/09/melatonin-and-seasonal-variability-of-ms.htmlThere is a search engine at the side if want to search if we have looked at the posts
Sorry, my bad. Thanks much for everything you guys do. Really appreciate this blog and all your hard work!
No association of multiple sclerosis activity and progression with EBV or tobacco use in BENEFIT.http://www.ncbi.nlm.nih.gov/pubmed/26453645
Hi Barts MS blog - don't mean to spam but would you be able to share our video promoting MS Decisions, the MS Trust's new independent interactive guide to MS drugs? We think it might be useful for readers of your blog - both MSers and health professionals. Video here: https://www.youtube.com/watch?v=_BAOf4GCoXE Thanks!
Could you pls. Profs. give your opinion about this news?Seems they have found an important causal factor to autoimmunity...."Study Identifies Blood Coagulation Protein Fibrinogen as Cause of Brain Autoimmunity"http://multiplesclerosisnewstoday.com/2015/10/14/study-identifies-blood-coagulation-protein-fibrinogen-cause-brain-autoimmunity/Thanks in advance
We published some work in this area 10 years ago. Sadly, neither have been cited in the study you mention.http://www.ncbi.nlm.nih.gov/pubmed/16049338http://www.ncbi.nlm.nih.gov/pubmed/17983428
Yes if you search the blog we posted on this a while back
Any comments?New study suggests quicker progression to SPMS if continue to smoke after MS diagnosis:http://archneur.jamanetwork.com/article.aspx?articleid=2432189Effect of Smoking Cessation on Multiple Sclerosis PrognosisJAMA Neurol. 2015;72(10):1117-1123. doi:10.1001/jamaneurol.2015.1788This study provides evidence that continued smoking is associated with an acceleration in time to SPMS and that those who quit fare better. Therefore, we propose that patients with MS should be advised to stop smoking once a diagnosis has been made, not only to lessen risks for comorbidities, but also to avoid aggravating MS-related disability.
It really is time to quit smoking !
Yep will see if ProfG is going to post this one
A colleague from my lab spotted a funny absurd thing on the NHS page about multiple sclerosis (http://www.nhs.uk/conditions/Multiple-sclerosis/Pages/Introduction.aspx). The second sentence: "Each nerve fibre in the brain and spinal cord is surrounded by a layer of protein called myelin, which protects the nerve and helps electrical signals from the brain travel to the rest of the body". For the ones that were sleeping during high-school biology classes: myelin are made of fat NOT of protein. She tried to signal this mistake but the site does not accept comment... BTW Thank you A.
My reading says myelin is made of protein and fatty substances.
Indeed there's a lot of fat but also proteins MOG, MAG, PLP etc. which are used to induce EAE.
I do not say that the cytoplasm of cells does not contain proteins (and I am pretty sure there are some mRNA and mitochondria here and there also) . What I say is that myelin is mostly made of fat NOT protein. I am sorry if I am pitiless with the NHS and I forget to add words to make a sentence correct when I read it ;)
This is interesting. Perhaps pharma greed may finally be getting its comeuppance.https://neurogram.wordpress.com/
"Democratic Party presidential candidates have mustered their outrage and called for regulatory controls, including proposals for requiring R&D expenditures to reach some minimum level restrictions on the deductibility of advertising costs tical imports from lower-cost countries; a reduction of marketing exclusivity for biologics; and the possibility of price controls"As much chance as Gun control? :0
What is the cookie name for this site that I can add to my exceptions list on google. My google chrome keeps crashing and the advice is to stop 3rd party cookies accessing my computer, but if I do this I can no longer comment on the blog, so I've had to open it up again to all 3rd party cookies
I wrote to my MP regarding the Off-Patent Drugs Bill. He is inclined to support it at second reading, but said in his reply that the Government is unlikely to support it, as the Health Secretary would then become a licensor of off-label medicines, which would result in conflict of interest: The Health Secretary would become an applicant in the medicines market, in addition to his role as overseer of the system. I don't know if the Accelerated Access Review and the Access to Medical Treatments (Innovation) Bill would do anything to mitigate failure of the Off-Patent Drugs Bill. All overly-complicated guff and gubbins to me, anyway.
I wrote to my MP a couple of years ago when the government were looking at car insurance. I'd forgotten to put I had a 3 year licence as drivers with MS have. When I added it, my premium went up immediately by over £200. I told him it was disability discrimination by the back door. He told me it was risk factor of the 3 year licence. We have them only because of our illness, not drunk driving. He gave me the same waffle used in your reply, but a year later my insurance went down by over £200. Coincidence? Who knows? At least you tried and anything that helps drive awareness to the people running this country is a good thing.
That's apalling. When I was first diagnosed, I was so nervous about the prospect of expensive car insurance, and these fears were not assuaged by the advice of a certain MS charity, nor by their offerings of special motor insurance for people with MS. But the fact is that a declared medical condition, as long as one has not been declared unfit to drive by a doctor, need make absolutely no difference to the premium. With a 3-year licence, I now have the cheapest insurance I ever had, going direct to the "Oh yes!" dog company (it's cheaper than what the MS charity's insurance would have been for me). I have been upfront about everything, but the insurance company took no interest in my diagnosis of MS. If you're considered medically fit to drive, you're fit to drive. End of.
Yes the law says they can't discriminate, that's why they were using the three year licence get out. Every company I tried was the same . That was the reason I wrote to my MP. I got the free dog with my insurance.
I started taking copaxone 40 mg about 10 months (29 yr male do 1 year ago). I just recently had an mri scan and it was stable (no acute relapses) and he said that was encouraging. The problem is that my symptoms have gotten worse (neurogenic bladder, back pain, very mild spasticity, and worsening nerve pain in legs). What in the world is going on? I'm really considering a stronger DMT. It's seems my inflammation per the mri is under control. But it feels there is something else going on. I am thankful that I do have the option to take fingolimod which I am strongly considering. Can anyway share if they have had a similar experience with their ms and how they handled it? Thanks much
Thought this was interesting Team G,Study observed those with vit D over 100nmol had less new lesions on MRI. http://www.ncbi.nlm.nih.gov/pubmed/26458124JAMA Neurol. 2015 Oct 12:1-8. doi: 10.1001/jamaneurol.2015.2742. [Epub ahead of print]Association of Vitamin D Levels With Multiple Sclerosis Activity and Progression in Patients Receiving Interferon Beta-1b.Results:Overall, average 25(OH)D levels in 1482 patients were significantly inversely correlated with the cumulative number of new active lesions between baseline and the last MRI, with a 50.0-nmol/L increase in serum 25(OH)D levels associated with a 31% lower rate of new lesions (relative rate [RR], 0.69; 95% CI, 0.55-0.86; P = .001). The lowest rate of new lesions was observed among patients with 25(OH)D levels greater than 100.0 nmol/L (RR, 0.53; 95% CI, 0.37-0.78; P = .002). No significant associations were found between 25(OH)D levels and change in brain volume, relapse rates, or EDSS scores. Results were consistent following adjustment for HLA-DRB1*15 or vitamin D-binding protein status.Conclusions and Relevance:Among patients with MS treated with interferon beta-1b, higher 25(OH)D levels were associated with lower rates of MS activity observed on MRI. Results for brain atrophy and clinical progression were more equival.Interesting note:The authors point out that serum 25(OH)D levels are a marker of sun exposure as well as vitamin D levels so it may be a beneficial effect of sun exposure that is causing the benefit for MS, effects that have nothing to do with vitamin D.
It's National Vitamin D Awareness week in the UK (19th - 25th Oct 2015).
Any news on the Study on Lisinopril for MS?
I searched here in the group about MS Pediatric read as a case of an english boy of 05 years diagnosed with MS... Read publications on EBV, MS and children, but not seen on MS Pediatric and Genetics or Vitamin D would be ... MS Pediatric part of a endophenotype the disease itself? ...Could epigenetic alterations in the intrauterine environment propitiate the appearance earlier of MS?
Alemtuzumab use in neuromyelitis optica spectrum disorders: a brief case series.http://www.ncbi.nlm.nih.gov/pubmed/26477020I just can't understand this. Why whoever on earth would treat someone with such ravaging disease which is known to be B-cell mediated with alemtuzumab? Is that ethical ?
B cells express CD52 it is a T and B cell depleter
Any research into Lemtrada recovery time? I went into it during a relapse, and it's been frustrating in the extreme to see non-relapse Lemmies pull away in recovery while I'm still mostly couchbound.
Both of you Team G talk of B cells and of course after that Roche did Ocrelizumabe ad for MSPP, which come the articles on them...http://stm.sciencemag.org/content/7/310/310ra166
I've just moved house and I've no nerves for keeping up with all of this at the moment. So T-Cell suppression is pointless in progressive MS. But B-Cell suppression is very possibly not, given that Ocrelizumab had some effect on PPMS?My gut feeling (i.e. random, baseless statement): Neuroprotectives are key in PPMS / SPMS. So we need the UK Government to sort out this off-patent drug problem. NOW.
Entirely agree with you. Neuroprotectives are key and we need re-purposing asap. I must admit I have my doubts that the current administration (or indeed any administration) has either the will or the expertise to move things forward.Hope the move is OK, it's VERY stressful in my experience.
I'll keep campaigning anyway - brings me back to my Greenpeace protest days. ;o) Ah, the days when I could walk a mile with a banner...Thanks: No disasters with the move thus far. Once the kettle and the tea were found, things got a lot better.
Guys - I know this goes against your morals, but if you can't get pharma funding for neuroprotective trials, could you not do it as a patient-funded trial? From interest on this blog, I hardly think you'd be short of applicants (in a population who, let's face it, have few other treatment options).I don't know how much it would cost, but considering that Richard Burt over at Chicago Northwestern has managed to get HSCT through 3 phases of FDA clinical trials without a jot of pharma funding - albeit charging £150k a pop - this clearly is a viable route to getting a therapy through trials.People are funding it via fundraising, insurance, etc.I'm not saying it's ideal - to some extent I get why you're ideologically against charging for an "unproven" treatment... But, if you're saying there's pretty compelling evidence that such an approach would work, and that pharma aren't doing it, surely this approach is better than the current status quo?If I had progressive MS, and for the sake of a couple of fundraisers I could get on a neuroprotective for a year and in the process be shortcutting a year of pharma/medical red tape, I'd be absolutely all over it.Or there's the old crowdfunding option.Just feels like we're here moaning about it, when it wouldn't actually be that hard to get at least a proof of concept funded by the people who have the disease.Yes, it shouldn't be that way... The government, MS Society, pharma or whoever should step in. But they're not. Or at least not anywhere near fast enough.Which is the lesser of two evils; Sitting on our hands and doing nothing, or asking patients to invest to find a treatment that could potentially save them - or at least rule it out so we don't spend another 50 years waiting to investigate a dud.
The problem with the Burt thing is it not controlled-trial so the people are really paying for a service which is dressed up as a trial and the other thing is that the trial is going very slowly.Could we set up a registry and let some people have access to drug. We tried this with Cladribine, which we knew worked, but they said no, so are they going to do this for something we dont know if it works.Next who is engaged enough to do this, OK we have been pushing neuroprotection, but lets look outside there is SMART which is UK wide and ongoing so there is a trial already ongoing. The simvastatin trial is currently too expensive to fund and then ther Neuros are spending their effort trying to compare this or that pharma drug.So it is not that things aren't happening they are they are just nt happening fast enoughHowever I do think we need patient power but whether we can do it in UK is another matter. In the US there is a culture of philantropic donation, more so in the the UK. We would really love to find a big donor for some projects because I fear this is the only option more on this to follow.The Brave Dreams Trial never got enough money via a crowd sourcing route. Whether crow sourcing can make the amount of money needed will be interesting to find out. I know if it is possible but you needinfracture to advertise and have we got enough time in a day on top of all the other things we do. There we need others to engage to do this as we can't do every thing. However what do you do it for the emotive stuff that is more science fiction?ProfG is speaking about street cred and attempting to get crowd sourcing has led to a few people turning up their noses.
"If I had progressive MS, and for the sake of a couple of fundraisers I could get on a neuroprotective for a year..."A couple of fundraisers? My, you must be a brilliant fundraiser! When I think back to my Greenpeace days and what people were willing to donate for "save the whale" campaigns etc.!!!
Thanks MD.Take your point re concerns over the Burt trial. My understanding was that it is controlled (crossover) controlled, but it's not blinded - which will perhaps be the issue. We shall see.Either way, doesn't change the fact that he's managed to get it through 3 phases without a jot of funding (I think it concludes next year) - and the blinded or not part is not relevant to that.Even if it moves slower than a pharma trial, it's still considerably faster than no trial at all. Proves it can be done, self funding, without benefactor or crowd-funding or pharma investment. I have great admiration for him for that. He's tried to get Pharma, they've said no, he's believed in it and gone for it. With pretty impressive results so far.Out of interest, who said no to the Cladribine trial? The European regulator? If it was set up as a proper trial, with a control arm, blinded, and patients self-funded their own participation, could/would they still say no?Also, presumably with neuroprotectives the associated morbidity risks would be much lower. I can imagine more tension about prescribing a high dose chemo drug versus a neuroprotective that has been proven safe elsewhere.I don't think you need to go down the sci-fi route (i.e. repair), but I think you're right that it needs to be the more emotive stuff/something with the prospect of being a game-changer. Neuroprotectives could be that, and are hardly sci-fi. Even EBV captures the attention. Or deleting OCBs. I'd love for you guys to have a small-scale, always-on "test and learn" lab, to rapidly test concepts in real patients - rather than all this red tape.Who are the people turning their noses up? Prof G shouldn't put too much weight on garnering the approval of the old-school neuros in my view. They've proven themselves to be less than useless in MS. Time for a change.
You may be interested I have met the UK HSCT arm.Anyway Who said No to CLAD...the MHRA. Academics can not afford to go to the EMA, at over £30,000 for a proper consultation.£3,000 for the MHRA. FYI MHRA said yes to another trial and said what they wanted and the answer to that was costed at about £3-4,000,000, if the NHS paid for the comparator drug. If they didn't add up to another £15-£17.5,000,000. So for cost of £4,000,000 ,the NHS would have saved £25-35,000,000 by doing ta study. Sadly no-one in power is interested!. Which is unbelievable!The cost for the CLAD was peanut and there would be the cost of MRI. The main cost is the staff to do the monitoring in multiple centres throughout the UK and the cost of dealing with side-eefects of the comparator. Some bits could have been pruned. More in the future.With regard a test and learn lab....the ethical process has put that to bed, but we are thinking of some testsAlso while we are discussing CLAD you may be interested to know that CLAD crosses the blood brain barrier (unlike other MS drugs), it is active on dividing and non-dividing lymphocytes and kills plasma cells and is reported to get rid of OCB. Who is turning up their nose?....Where do I start......but you may be interested to know that ProfG is on the dark side with his nose in the air on this one:-(.. Shocked?
ProfG. I am indeed shocked.
We cannot just give up on the Government. Enough people making enough well-reasoned and -informed noise can achieve great things. To say that the Government is currently incapable may be stating the truth, but it also promotes the very lethargy that constipates the Off-Patent Drug Bill. Change is required, but change needs pressure and a lot of badgering. I personally certainly do not have the funding to take part in a trial, nor the insurance. And fundraising doesn't seem realistic either. I know of many with a lot more physical energy than I who go hell-for-leather and manage to raise a hundred pounds here or a couple of grand there for worthy medical causes. Nowhere near enough.
MD - You met the UK HSCT arm? As in Dr Snowden and co? Cool. What was the outcome/your thoughts?Re your points on Clad, I'd love to see it get licensed - sounds like a no brainer. Especially if it crosses the BBB and is active on plasma cells. If it was available (or on trial) and reasonably safe (which it seems to be), I'd definitely take it post-HSCT just to cover all the bases. I reckon I'll probably go for some kind of anti-plasma cell treatment in the next 5 years one way or the other (either on trial if available, or private if not).I know I've harped on about this before, but do we really still need comparator drugs in this day and age? Surely from previous trials there's a huge database of what natural (untreated) history looks like, and the same for all the licensed therapies too. And given that that data will be on much larger scale than the control groups on any individual trial, it would have better statistical significance as well and be less subject to skewing by an over/under-performing control group. No brainer?!If the risk is that the cohort will be selected with bias, why don't they just appoint an independent body to select the participants? Save an absolute fortune.And with MRI, VEP, atrophy, neurofilaments, functional measures, immune profiling, etc. surely there's enough quantitative measures to say whether a treatment is working or not beyond the "placebo effect", without blinding/controls. Works OK for cancer.
Hey SterntaucherSorry - I didn't mean to be flippant about the fundraising thing. Appreciate money doesn't grow on trees. I'm just basing it on HSCT where there's a community of hundreds of us who have had it done overseas, privately funded at tens of thousands of pounds. All just ordinary people, not millionaires.A lot of it is savings/family/etc. I'm sure, but some have raised the whole thing via a concerted fund-raising effort over a couple of years. Pretty amazing.Not saying this is possible for everyone,I'm just saying if there was a self-funded (within reason) neuroprotective trial that had a serious prospect of halting/substantially slowing progressive disease - and it was open to those with early disease (i.e. still in full time employment), I doubt there would be a shortage of applicants.And, in the long run, getting the trials done now would be in the interests of everyone in the long run - even if it goes against the socialist ethos of the NHS. If people are willing to pay for it, and it progresses the field and speeds things up, all the better in my view.
MD - Sorry last question. Why is ProfG against Crowdfunding? What if we throw in a Limo? :-)
Not against crowdfunding, but against developing treatments without pharma involvement:-(
Hi Matt, Your suggestion is intelligent and reasoned and certainly worthy of consideration. But I think that some people being able to afford to take part in trials and others not would encourage polarisation of the "haves" and the "have nots", quite possibly promoting the creeping privatisation of the NHS. I'm also very sceptical about how readily the benefits would trickle down to those who cannot afford to pay.
I know that we must be judicious with the studies we read publications, and I know also the specific study is also based on differentiating T cells, but what would be the true "weight" in diets rich in long-chain fatty acids, especially for who has MS? Because I always spread that they would be anti-inflammatory, and hardly anyone flies quote the contrary ... http://www.cell.com/immunity/abstract/S1074-7613(15)00392-1
I have been too busy to read the paper and was waiting for the link to appear in pubmed but will post on this when I have read this paper and seen the quality of experiments but there is their any quality control. On first glance the control groups are vastly different in some of the experiments....does that bother you it does me.
Thank MD. But I was very interested in your comment above on Cladribine actually reach the brain and erase the OCBs. ... If I could actually pick certainly would opt for CLAD as a treatment option. Is there a study evaluating treatment together CLAD and Copaxone?
At the moment CLAD is not a licenced option and the effect on OCB needs repeating. I don't know of a study evaluating CLAD and cop but based on published data I am not sure why you would want to take COP as CLAD will be over twice as effective. However there was once a study by Mike Boggild based on our tolerance idea of immune deplete followed by tolerogenic antigen and he used a single dose of mitoxantrone followied by COP and there were essentially no relapses afterwards. I could never understand why Teva did not follow this up maybe the cancer risk with mitoxantrone
Yeah I know that CLAD is not yet licensed for the treatment of MS but I think it really was something to Teva consider a adicioinal treatment CLAD and Copaxone and see what would ... I read somewhere that Genzyme was considering the possibility of testing alemtuzumab followed by the use of Copaxone, not only saved the link of publication ...
Why would they use copaxone with alemtuzumab as they have aubagio unless teva are buying sanofi:-)
Because of the tolerogenic effect post-depletion, which you referred to above?
Oops I forgot to mention in the question I asked above this list would also be fitted long-chain polyunsaturated fatty acids, which are regarded as anti inflammatory ...
Hey Team G.I've been thinking some more about Prof G and his plasma cell theory, alongside the research that shows Natalizumab (10 infusions+) seems to reduce OCBs to below detectable levels.Would it be possible to analyse the impact of induction therapies on those patients who have already had long term Natalizumab therapy (or vice versa)?I.e. Assuming that a reasonable percentage of long-term Tysabri patients have been rendered OCB-negative, do they do better after an induction therapy than those who have not had Tysabri (and are thereby, most likely, OCB positive)?Would be interesting to look into the stats, perhaps, for a sneak-peak (albeit not conclusive) into whether the deletion of OCBs is clinically significant...If the data isn't there from the Lemtrada trials, I bet it is there from some of the HSCT trials, as the entry criteria for a lot of the early HSCT trials was that you had failed 2nd line therapy (and the control arm from Richard Burt's MIST trial is mostly Tysabri. As it's a crossover trial, this data is surely sitting there...Worth a look?Also, any news on that Elotuzumab thing? I'm impatient, I know! :-)Matt
I think ProfG believes the natalizumab stuff needs repeating. Most people on natalizumab will not know anything because most people will nt be volunteering to have their OCB checked. They may get a diagnostic LP at diagnosis but theyare not going to have others for no reason so you have to get ethics and do the study and hope people will have an LP. They wont you would have to contact Dr BurtWith regard Lemtrada the data seems to be that OCB remain present in the people they have looked at.As to Elotuzumab no news that can be made public . However there are easier and to target plasma cells we believe and are looking in to this. Data suggests this can get rid of OCB.
Thanks MD.If you do get a anti-plasma cell trial going, let me know. I'd probably apply if eligible.
We are discussing one. Will see how much energy we have as we have alot of balls in the air and need more catchers on the ground so we don't let them drop.
Montelukast - any interest or investigations going in MS? Is this a neuro-protective? Looks interesting from the DailyMail write-up, but always have to take that with a pinch of salt.http://www.dailymail.co.uk/sciencetech/article-3290482/The-wonder-pill-STOP-ageing-Common-asthma-drug-cure-Alzheimer-s-claims-study.html
If it claims cure in the Daily Mail change this for crap reporting & false hope any wayMontelukast is a leukotriene receptor antagonist (LTRA) used for the maintenance treatment of asthma . They have done some tests in rats and found that it aids some behaviours affected by aging. There was a study of this drug in EAE and as an immune modulator its effects are modest, but could it be neuroprotective, possible. I'll wait to see more data.Also this is work in a rat.clinical trials only revealed an increased risk of insomnia, post-marketing surveillance showed that the drugs are associated with a possible increase in suicidal behavior and other side effects such as agitation, aggression, anxiousness, dream abnormalities and hallucinations, depression, irritability, restlessness, and tremor...great for MS...not
Very aggressive side effects ... I'm hoping that the MS-Smart trial to Amiloride and Fluoxetine to work, including as a neuroprotective ...
Team G, Do any anti anxiety medicines help reduce MS symptoms in anyway?
On BBC websiteMultiple sclerosis patient walks after taking HIV drugshttp://www.bbc.co.uk/news/uk-england-sussex-34659771
Maybe they just need to publish the results of the trial of the single anti-HIV drug
Yes but from what I understand this MS patient was on a combination of HIV drugs.
I know of a case in Brazil of a woman with HIV who was later diagnosed with MS ... Just I don't know if she started antiretroviral treatment ...
So a spokeswoman from the MS Society made a comment. Perhaps the MS Society could help with funding for this research, if further funding is needed?
They write about Prof. Gold as well. If what they say is the truth, it is simply marvelous, too marvelous to stay hidden and secret.MD. can you confirm the case they are talking about?
An anti-viral. Guess it is a plus for the viral theory.
The effect of HAART on MS was reported as a case result 4 years ago and I do not understand why this is hitting the news. Proper science studies need to be done and without that the anecdote is interesting but nothing more than that.
I guess there's been some fur flying ;-) The post relating to hiv drugs and the media clip seems to have been removed. Hope to see unity restored and glad to see it's not a case of do as I say and not as I do ? If you see what I mean ?Catch you later , gone fishing :-)Regards as always
Well spotted Andy. Yes, normal service has now been resumed.Enjoy the fishing.
Eucalyptus oil contains high levels of viral integrase inhibitors. Raltegravir is an integrase inhibitor. Thought it was interesting.
Would be a clue linking EBV infection, genes and autoimmunity? http://www.cell.com/ajhg/abstract/S0002-9297(15)00372-9
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