Please may I ask, how do the blog authors manage to keep on keep on top of all the latest MS research?
By not sleeping ;-)
Is there anything exciting we should be looking out for at AAN?
Well there'll be some lavish Pharma stands for a start.
The program is online...
This has doubtless been covered previously but I couldn't find it using the search tool; what is the evidence for / benefit of hyperbaric oxygen therapy? Please enlighten me or point me in the right direction thanks :-)
I dont think we have anything. As a DMT is has apparently been put to the sword, symptom control maybe
Thanks for the heads up on HBOT, I didn't know they did control trials on it for MS. Here's some papers I found on it. http://www.ncbi.nlm.nih.gov/pubmed/7639061This paper is from 1995 http://www.ncbi.nlm.nih.gov/pubmed/20415839This one from 2010.
Hyperbaric oxygen was a fad before my time. Based on recent data an argument for oxygen doesn't have to be pressurised can be made on grounds of countering tissue hypoxia. However this has not been substantiated in a clinical trial.
If you put oxygen in the search bar you'll find that we have posted on this a few times.
Bart's team, if you could, please review and provide constructive criticism of the study, Neuregulin-1 Controls An Endogenous Repair Mechanism After Spinal Cord Injury, was a collaborative effort between researchers from King’s College London and the University of Oxford, and published in the journal Brain. This seems very promising to MS patients with respect to remyelination and neuroregeneration.
I'll have a look next week if I can find the time
I researched Neuregulin 10 years ago, these are endogenous proteins and the in humans there are several forms of it highlighting its imporatance in the CNS.
NDG, why did you stop working in neuroregulins? Can you comment on the progress over 10 years since you studied them?
I didn't exactly stop working on them, but the overall interest of MS scientific community is focussed on neurodegeneration. In MS there has been little progress in endogenous repair mechanisms as a whole, majority of the work is in spinal cord injury and attempts to translate into humans have failed as its a complex system. If you look at even a handful of patients the differences in isoform paterns for neuregulin is big - some had up to 11 whilst others had ~5. I'm hoping to have new data on regenerative biomarkers for ECTRIMs - so watch this space!
This may be inappropriate, I hope not but I would really love to know. If your child were to be diagnosed with RRMS, what would your course of action be? What treatment would you want them to go on? Thank you,From someone's daughter just diagnosed with RRMS.
I don't have any children that I know of:-)This hypothetical. I would want the most effective treatment available and the best way to find out what options there is to seen by a specialist in paedeactric MS. I know there are such people at Great Ormond Street Hospital. I appreciate that this is a worrying time but each case has its own issues which dictate the best treatment course. ProfG has done posts for questions you should be asking the neurologists if you have MS. You need to ask what is you JC virus status.
Re:HBOT thanks, have Googled and understand principles. What bothers me is that, as MS is autoimmune disease, increasing supply of oxygen to cells could HELP the disease process?
Re: "...as MS is autoimmune disease,..." This is uncertain, the cause is still unknown.
Here is an interesting study in Alzheimers:http://science.sciencemag.org/content/early/2016/03/30/science.aad8373Synapses attacked by complement and microglia, well before the plaques develop. Can something similar happen in MS?
Sure could I'll have a look next week
Re Lemtrada (Alemtuzumab):If patients have taken Alemtuzumab early with a low lesion load and no disability, remain stable but after many years still transition to SPMS... Do they not fair better considering they enter this phase with minimal damage & no disability? And if the theory that existing sites of damage provide the location for neurodegeneration later, could the patient expect to not experience debilitating symptoms if their initial symptoms were minor & sensory?
Although MRI changes can predict early disease outcomes, progression between individuals is still variable. Early motor symptoms have been shown many times to be poorer prognostically.
Motor symptoms in MS include muscle stiffness or spasm, muscle weakness, difficulty walking and tremors. Are there any other motor symptoms I've not listed?
Predominately we mean weakness - as its a fair indicator of long tract signs, which have a large degree of redundancy in them but once the signs are there all the time the capacity to compensate is less. Disability therefore becomes increasingly evident.
Can I ask what the big fear is with Lemtrada? All secondary AI diseases respond well to treatment *if detected early*.
The big fear for lemtrada is ocreluzimab:-)
Ha, unlikely. Not as a maintenance treatment anyway. And who knows the long term effects of continued B-cell suppression. And given that rituximab did little to delay the onset of SPMS (granted it perhaps wasn't given early enough) I'd rather put my eggs in the Lemtrada basket & rebuild from the bottom up
My previous comments on EBV vaccination felt like a whisper in the crowd (saturday morning lyrism). A vaccine for the herpes virus does exist. Wouldn't it be a good idead to vaccinate MSers?
The idea of vaccinating is to lessen the effects of the infection when you're exposed to it in reality. Very little point once you're already exposed as the immune response has already formed.You'd have to do this at a young age, since a large proportion of the population are exposed to this, this would be a mass vaccination programme...
If I understand you correctly, you think that the already existing vaccination program of the elderly (70 and 78) against Herpes zoster (http://www.nhs.uk/conditions/Shingles/Pages/Introduction.aspx) has "very little point"? Interesting. I think, however, that vaccinating a few MSers is not "mass vaccination programme". In the following paper they talk (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC404574/) (in the abstract) of therapeutic effect and not only prophylactic.
Not everyone is exposed to herpes, where people are seronegative (ie no evidence of immune response to herpes in their blood) it makes sense to vaccinate. We do this for fingolimod and VZV. Now what you're asking for is a therapeutic vaccine. The HSV reactivation and reasons for it are based on lack of proinflammatory (Th1) activity on the background of a normal immune system. You can develop a vaccine which boosts this Th1 response leading to an immune response which kills the virus as it reactivates. In MS you definitely don't want to boost a generic proinflammatory response. There needs to be a way of making this an EBV only response without the fall out. Do we know why EBV reactivates firstly?
You vaccinate people before they start fingolimod (all of them?)? And you vaccinate people with the Varicella Zoster Virus (VZV) - what's the point (given your opinion) if they are already infected. BTW this article discuss about the link between this virus and MS http://www.hindawi.com/journals/msi/2011/214763/ maybe you already commented on it. Behind your last question (that I share) there is a strong assumption. Do you think that relapses are due to an EBV reactivation? In this case antiviral during a relapse should be effective, no?
Not much has happened since ocrelizumab. I guess we have come to a standstill. Repair is a long road. Only phase 1a trials so far. Sigh..
Not true...I know of phase IILaquinimod has hit problems since news of ocreluzimab...I think this is bad news for people with MS as it probably is a neuroprotective agent...the heart side effect is its down fall as the therapeutic window is going to be too small.
What I don't get is this; If MS is a B cell disease (according to the new dogma), then how is it that Alemtuzumab - which targets mostly T cells but quite a lot of B cells too - is an induction therapy that puts patients into years of remission.... Yet a Ocrelizumab wipes out more B cells and needs top ups. If the B cell is the problem, surely you'd expect the treatment that targets them more completely to have longer lasting/higher efficacy?
Well spotted if MS was B cell driven then we would need alemtuzumab every 6 months as the B cells are bad to normal within 6 months. T cells on the other hand are wiped out of sight for a long time and this better equates to the treatment effect and the induction effect. Maybe the new dogma is mushroom food(a) Does ocrelizumab really need top-ups or could it too be an induction therapy. Will this data surface? Once 6 monthly is a better business model than two doses a lifetime:-(.50% of people taking alemtuzumab need top-ups.W(b) Is it true that alemtuzumab miss the Bcells. I saw a poster at ectrims showing CD19+, CD5+ B cells transiently dropping followed by over shoot whereas CD19+, CD27+ B cells showing long-term depletion.The answer is in there and the break through of antigen reactivity should give us a clue, NIHR were not interested in funding study to bank the sames because disease causing cells must retrun before disease retruns
Can I ask what is probably a very basic question; When a patient becomes SPMS, generally they cease to have new acute lesions on MRI. What mechanism causes this to stop? I get the theories around progressive being simply a loss of reserve capacity - which makes sense - except I don't understand why that would result in quieter MRI/acute attacks. Please could you explain?Thanks!
Good question and I don''t know the answer. We see this burn out of attacks in the beasties too as well as MS. There is still myelin there to attack there are still oligodendrocytes to attack. The animals are older, different genetics means different number of attacks different sex means differnt nconsequnces of attacks.If we go down the epitope spread route we go from one epitope to another should it exhaust itself.
It's tempting to speculate that adaptive immune response in MS actually protects against progression - but only up to a point.
The inflammatory acitivty is still present in SPMS at least in the CSF, OCBs in particular. Maybe the disease changes into something else as it evolves and the MRI is not picking it up?
There is a recent article in the Journal of Neuroscience, unfortunately dated 1st April 2015, that discusses Mitochondria and their effect on progressive MS. http://www.jneurosci.org/content/35/13/5293.full.pdf+htmlThe article discusses the progression of the disease, and how a treatment can have a different effect on the axons depending on the length of time the disease has been present.Interestingly, it also includes reference to how the EAE model is not always applicable to human MS.Has this article generated any follow-up research?
Well forgive me for my immodesty but we published on this very subject including a therapeutic benefit from a compound we made, recently. We think our EAE model is a pretty good correlate of MS.http://www.jbc.org/content/291/9/4356.long
Excellent news MD2! It would be brilliant if we SPMS sufferers could benefit sooner rather than later from all your work. The article I mentioned covered a different aspect of mitochondria, so I'm pleased that these little organelles are generating so much interest in your community. They get involved in RRMS as well as SPMS, have connections to vitamin D, and to viruses, so hopefully they give researchers a lot of new avenues to explore. (Even if EAE was not so perfectly compatible in the 1st April article!)
CRISPR technology is a powerful tool used for gene editing. With all the speculation that latent EBV is driving the inflammatory process in MS has there been any studies on removing the EBV DNA from B cells in MS patients? There is quite a lot of excitement that latent HIV can be eliminated or at least drastically reduced using CRISPR.http://www.umassmed.edu/news/news-archives/2015/04/editing-hiv-out-of-our-genome-with-crispr/
Dimethyl Fumarate acting on B cells?!http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4784801/
Yep any self respecting DMT will now work on B cells as MS becomes a B cell centric disease with the advent of ocrelizumab, we have already had the copaxone works on B cell paper;-)
https://www.youtube.com/watch?v=MnYppmstxIs&ebc=ANyPxKqdCh4uCtOjE5umXQPIyPSNp7j4zhUHHTDCzMnyJJ4whatjkH3MkrUzHCuGGrEDuAiqVulfIxD_O0LVLUyfmcrXuHhNnQ&nohtml5=FalseThis is a good overview of CRISPR. Scientists will be able to modify our DNA and thereby correct genetic mutations responsible for disease. If there are viral genes responsible for MS inflammation then theoretically they can be removed and replaced. There has been use of anti-viral meds in clinical trials for MS but why not just delete the viral nucleic acid just as bacterial cells do with bacteriophages?
I went to a talk yesterday in my new work place: Cannabinoid-induced actomyosin contraction shapes neuronal structure and connectivity at multiple spatiotemporal scales"""Abstract:We have recently shown rapid cannabinoid-induced remodeling of the neuronal actomyosin cytoskeleton with potentially important roles in developmental brain wiring. Our recent results indicate a role for cannabinoid-induced actomyosin contraction also in synaptic plasticity. I will also present how we complete our in vitro and ex vivo tools by participating in the interdisciplinary development of a new in vivo imaging modality, functional fast brain ultrasound (fUS), to investigate the role of cannabinoid-induced actomyosin contraction in the structure and connectivity of the living rodent brain. fUS offers fMRI-like functional imaging, both in anaesthetised and awake animals, with spatio-temporal resolution gains of several orders of magnitude as compared to fMRI.Main recent publications:Renard et al. Eur Neuropsychopharmacol. 2015Chatelin et al. Journal of Cerebral Blood Flow and Metabolism, 2015Errico et al. Nature, 2015Ladarre et al. Frontiers in Cellular Neuroscience, 2015Roland et al. eLife, 2014Osmanski et al. Nature Communications, 2014Simon et al. J Mol Cell Biol. 2013Thibault et al. Cerebral Cortex. 2013"""They are doing some impressive things in ESPCI (former lab of Marie Curie). I discussed with the speaker. They are currently doing work on the role of cannabinoid and bilirubin in axon guidance. Properly fascinating, he told me that they file a patent for this molecule in the use for MS. This is another piece to the puzzling effect of THC based drugs. Their effect is not only myorelaxing but they also might play a role in axon guidance during their growth. What do you think?Strange feeling to be in the front seat of your own disease research.
very interesting but hopefully they are not using CB1-based drugs as they have side effect potential man the ROCK pathway.
Thanks for sharing - very interesting! I agree it's a strange feeling to go to a research presentation on your disease - I've been to a talk by one of the discoverers of the DMT I am currently taking; it was at a rather large meeting, and I did not approach the speaker (perhaps a mistake).
Came across this self Sit to Rise test on the BBC today to test balance and core strength, to test our age. It shows how good our muscles are. I'm 41 with RRMS and I could get down ok but getting up I was all over the shop. It's harder than you think. I walk 20 mins a day. http://www.bbc.co.uk/programmes/p03q0jrw?intc_type=singletheme&intc_location=avs&intc_campaign=bbcone_howtostayyoung&intc_linkname=vidclip_standyourage_contentcard4
Typiical BBC science stuff no real punchline information. and pseudo science. The experiment had three dogs two dogs made owners relax and one didn't so there is no effect of dogs on a sample size of three..complete and utter misleading tosh...on age and body next week age and brain health next week w
There is an easier way to do the Sit and Rise test I have worked out. The first time I did it I failed. When you are ready to rise you swing you body back a bit further and that motion helps get you to rise easier.
There was discussion about this on BBC Radio and a yoga teacher phoned in to say the Sitting and Rising test is not good to do as it can damage the hips.
http://www.fool.com/investing/general/2016/04/10/after-nearly-39-million-deaths-a-cure-for-hiv-coul.aspxProf G, since you are a proponent of EBV causing MS, why can't latent EBV DNA be eliminated from B-cells using the same technology (CRISPR) as is planned for latent HIV and end the controversy of chronic EBV and MS? This seems like it should be a "no-brainer" in MS research.
It would be the "EAE cure" of March? Cyclotides from plants for example coffee, cucurbits or even grasses and the nightshade family of plants. In this study the cyclotide was removed from Kalata-Kalata (Oldenlandia affinis), and it seems that Kalata B1 suppressed interleukin-2 messenger substance and therefore the division of T cells, which act as "killer" cells or "helper" in response to the human immune system ... Still looking only for T cells... Even so this would be a further mechanism by which the cafe action would reduce the progression of MS?http://m.medicalxpress.com/news/2016-03-peptide-onset-multiple-sclerosis.htmlhttp://m.pnas.org/content/early/2016/03/22/1519960113
The problem with botanical chemical being used is that the dose bears no relationship to the amount in the plant so the correlation is irrelevant.Looking at the claims in medscape "The one-off oral administration of the active agent brought about a great improvement in symptoms". has been done many many times before with agents that look much better...so yep candidate fo MS cure of the week.
Thanks MD, and would be "coffee" instead of "cafe", the neurons here sometimes come in "short circuit" and want to mix portuguese with english...
A deficiency of vitamin D leads to excessive response of B cells?! ...http://www.nature.com/nrneurol/journal/vaop/ncurrent/full/nrneurol.2016.49.html
Mouse Doc, did you posed for this sculpture?https://commons.wikimedia.org/wiki/Category:Monument_to_lab_mouse#/media/File:Monument_to_lab_mouse-1.JPG
Luv it, Luv it, Luv it.
This may have been discussed before but does smoking reduce the efficacy of MS DMT's?I was at a discussion today on RA drugs and the expert mentioned smoking can half the efficacy of RA drugs.
Does it matter when smoking is a known risk factor for MS, cancer, tarred lungs, bad skin, bad breath, yellowed fingers and hair, cardiovascular disease and when it makes a person stink?
I think it's a good enough question to ask. I don't smoke but I imagine some RRMSers on a DMT do continue to smoke. Even though they know it has a risk factor for the things you mention.
I'm not sure I want to ask this question. Can MS affect the heart?
Yes, I've lost a lot of my heart to this disease:-(
Can MS neurologically affect the heart muscle?
I would have thought brainstem relapses could impact on the heart? The midbrain that regulates involuntary functions such as heart rate, and breathing rate.
Seem to have found the answer to my own question myself - yes. Drastically.http://www.ncbi.nlm.nih.gov/pubmed/21586485
Yes, active demyelination of the medulla oblongata, part of the brainstem. I was thinking that sleep apnea and snoring can impact on the heart, it's not good for the heart. Sleep apnea can be associated with damage to the brainstem.
How Do you Anticipate Ocrelizumab Will Be Used In Treating rrms? Will it be considered a 3rd line therapy like lemtrada? Since it is supposed to be highly effective in rrms and somewhat effective in ppms and not associated with pml, doesn't it render most other therapies useless aside from maybe Lemtrada?
I would think first line would be the desire. In UK will make it second line but if lemtrada can get first line there would be no justification for it not to be first line as it is effective and does not have secondary autoimmunity potential
Thanks md. Sounds like it will be a real game changer in treating rrms if/when approved (especially if used as first line). And hopefully a good chunk of progressive ms' ers will have some response to the therapy as well.
"it is effective and does not have secondary autoimmunity potential"Just a little increased cancer risk and immunoscenesence. And no answer to how long this drug could/must be used for. Nothing to worry about - just quaff it down and see, eh.
This has been refuted before and no doubt will have to be again but thanks for visiting.
MD2 was talking about cladribine I thing this is the response when you mention cancer risk. Any immunosuppressive agent carries this risk but as to length of time you use it for. Depends on how long it is before you switch to cladribine :-)
Heaven forbid a criticism of the holy Cladribine. That would be heresy.
Heresy might be a bit strong, misguided perhaps.
Well if you become defensive in the face of misguided criticism, that gives a bad impression. If you were a door-to-door broom salesman and I didn't like the bristles on your brush, you wouldn't have to take the huff. Just sell it to someone else if it's that good.
You cannot say that Cladribine is beyond criticism. That is not honest.
Well the proof will be in the pudding, won't it?
Nothing is beyond criticism. even me:-).I was criticised for making this post because it advertises to everyone when the Merck posters are no need to look in the absract book:-(
Didn't Prof G himself on this very blog say in one of his comments that people are concerned about immunosenescence with Cladribine? MD2 - you sound really grouchy.
"Brain doctor 'sent naked selfie video to patient he was having improper affair with'"I got worried when I saw this news headline. Thankfully, nothing to do with Mouse Doctor (I knew in my heart it wasn't you MD).
Yes not me I say keep it in your pants but there is a naked selfie on the blog if you want to be put off your breakfast:-)
Those are yet to be published, so behave everyone or they will be ;-)
Like my dentist said to me they do things a bit differently in Norfolk.
Has anyone looked at the therapy with Cladribine, followed by monitoring of vitamin D dosages and serology for EBV, before and after treatment with Cladribine?
No that I know of but may this can be put on the things to do list.I know that ProfG has been very interested in this post alemtuzumab.There is an interesting case study but a certain person does not want to publish it:-(
Gut bacteria regulate insulation of nerve fibres in the brain. "Research suggests gut bacteria may directly affect brain structure and function, and could offer new ways to treat multiple sclerosis and psychiatric conditions."Hoban, A. E., et al. (2016). Regulation of prefrontal cortex myelination by the microbiota. Transl. Psychiatry, DOI: 10.1038/tp.2016.42
Thanks I have been meaning to post on this for past couple of weeks but haven't had the time, maybe I will try this weekend
After watching the documentary How to stay young on brain health last night I was slightly depressed. Walking everyday, learning a new skill, and socialising was the best way to prevent our brains shrinking and helps new cell growth. Are we with ms who are unable to consistently do these things dommed anyway to lose even more. I would be interested in hearing if any of the techniques and trials showed would help us with ms, particularly brain stimualtion and giving young blood to people with early dementia. Anyway for anyone who watched im off to buy blackcurrants....
Restoring cortical control of functional movement in a human with quadriplegiaChad E. Bouton, Ammar Shaikhouni, Nicholas V. Annetta, Marcia A. Bockbrader, David A. Friedenberg, Dylan M. Nielson, Gaurav Sharma, Per B. Sederberg, Bradley C. Glenn, W. Jerry Mysiw, Austin G. Morgan, Milind Deogaonkar & Ali R. RezaiAffiliationsContributionsCorresponding authorsNature (2016) doi:10.1038/nature17435
I was surprised to see that New Zealand is an unrepresented country (grey)on the Brain Health Time Matters in MS map of the world.
Yer come on. You can beat us a rugby...now beat us with your commitment to brain health! However I think I was told by one of the neuros here that they don't both with the CRAB drugs in NZ you are straight onto the high actives.So maybe they will just tell me to close my piehole:-)
From what I've been reading they have maintenance drugs, that include DMF, Teriflunomide, Natalizumab and Fingolimod and all can be first line therapies. Also Avonex, Betaferon and Copaxone. But induction therapies are not mentioned.
Alemtuzub and HSCT are induction therapies
The MS Society of New Zealand do not mention alemtuzumab in their list of current MS treatments available. HSTC is listed under alternative therapies. http://www.msnz.org.nz/Page.aspx?pid=296
The two main antiviral flu medicines used in the NHS are:Tamiflu ( oseltamivir)Relenza ( zanamivir)Could these be useful in treating MS?Has any
Prof G - I'm somewhat bemused and confused and wondering if my eyes are deceiving me!E-mails and webpages from Professor George Jelinek's OMS program are publicising a new and revised but yet to be released edition of Prof J's diet and lifestyle book for treating MS and loudly proclaiming "We are thrilled to have the support of one of the most influential MS researchers in the world for this new edition, Professor Gavin Giovannoni, MBBCh, PhD, FCP (S.A., Neurol.), FRCP, FRCPath, Chair of Neurology, Blizard Institute, Barts and The London School of Medicine and Dentistry. Professor Giovannoni writes: ‘I would have no hesitation in recommending Overcoming Multiple Sclerosis to my patients, but also to my friends and colleagues.’While the "vegan with fish" OMS approach is focussed very strongly on maximum avoidance of saturated fats and animal protein sources, and strictly no dairy products, it does have some sound principles such as eat more fruit and veg, avoid processed foods, do more exercise and address other unhealthy lifestyle factors such as stress etc (all of which the general population would do well to adopt). It also encourages mega-dosing with Vit D - with many followers being self-proclaimed Vit D experts and recommending to others that they take doses of 100,000 or more units of Vit D, even when people have levels which are considered quite adequate or even high by mainstream medicine.However it seems strange to me that with your own declared support for newer studies supporting HF/HP/LC dietary approaches you would be unhesitatingly recommending an approach to diet which is so opposite.Not only that, but in relation to Alemtuzumab Prof Jelinek stated only a couple of years ago a view which is basically diametrically opposed to your "Hit hard, hit early" treatment philosophy:"I find it amazing that people with any illness would consider taking a drug that is so toxic. Alemtuzumab is a potent trigger of autoimmunity. Up to 1/3 of people taking it develop Grave's Disease, an autoimmune condition of the thyroid. In the major clinical trial, two people in the treatment group developed thyroid cancer. A significant number developed another autoimmune condition, idiopathic thrombocytopaenic purpura (ITP), a disease often resulting in severe bleeding due to a low platelet count. One in six people got herpes infections. I am very surprised that the drug has been approved in Europe. If anyone is offered this drug, make sure to ask carefully about side effects. Someone with very aggressive MS might consider the drug, but of all the MS drugs, it appears to have the most side effects"No wonder I'm bemused and confused! So, have you made comments about the OMS approach and/or the new OMS book which are being "re-phrased" or taken out of context?
OMS is about wellness and a lifestyle and an approach to living with MS. My take on this is that he is offering a guide on how to live well, regardless of whether you have MS or not. I just wish I had his self-discipline. Please note he is not promoting his OMS programme in place of conventional MS treatments. Therefore we will continue to disagree on my approach to treating MS. The problem is that most readers assume his OMS is a treatment for MS when it is not. For OMS to be a treatment for MS he would need to do a randomised controlled trial and get it licensed via the regulators.
Paper presented the AAN about a possible neuroprotective effect of Alpha Lipoic Acid... Yep, it nutraceuticals, the great problem of concentration vs. dose, but it reminded me of N-Acetyl-Cysteine...http://www.neurologyadvisor.com/aan-2016-coverage/potential-treatment-benefit-of-lipoic-acid-in-ms/article/490542/
Demyelination of the medulla oblongata has got to be in the top five most devastating locations in the brain and spine. That and locations that can cause weakness in the legs.What do you think Team G? I would be interested to know your thoughts on this.
The medulla oblongata (or medulla) is located in the hindbrain, anterior to the cerebellum. The medulla oblongata is a cone-shaped neuronal mass responsible for multiple involuntary functions ranging from vomiting to sneezing. The medulla contains the cardiac, respiratory, vomiting and vasomotor centers and therefore deals with the functions of breathing, heart rate and blood pressure
Sorry I should of explained better, I know this about the location of the medulla and what it does.What I would like to know is what do your team think are the most devastating locations lesions can be in the brain and spine?thanksI would say the medulla is my top number one.
Prof G I wonder if there could be a role for peer support in MS care? I was reading the MS Forward View details about a shortage of MS nurses and care for those especially with progressive MS.I am not saying that peer support would replace a small proportion of MS nurses but peer support is becoming increasing vital and used in mental health care. When I was diagnosed with MS I didn't know anyone with MS and I first met an MSer over a year later. I know there are MS treatment centres and societies in some areas (not that near me though) and MS helplines but it would of been good in some ways to meet in person an MSer in a peer support role fairly soon after my diagnosis. Helen
Guess this is a good piece of news, worth looking a the PNAS article in more details. http://www.sciencealert.com/scientists-just-got-a-step-closer-to-creating-a-universal-treatment-for-allergies
Thanks great news let's try it. This is a story that the guys from Chicago have been treating Th2 allergies with nano particles. I don't have my computer so can't comment. We have been saying forever that Th1 = bad, Th2 = bad we don't want either and intravenous tolerance is the way to go to get antigen specific tolerance. Do we need nano..I suspect no, based on the Chicago and others work, but funny how approach of beads and antigens can induce allergies when the approach using cells was reported to get rid autoimmunity by supporting Th2.Will this approach be useful in MS.only if we know what the targets are.
After apparently concentrating on MS for so long, Steve Miller seems to be now flitting between various immune disorders like a butterfly in summer.
This seems to correlate with some people's perception of the "dead end" in curent MS/immunology research. Still no antigen identified. Larry Steinman called for a focus on NMO in attempts to develop tolerance. Biogen seems to be shifting towards Alzheimers. By the way, I personally think that huge progress has been made, and new dicsoveries are certainly going to be seen in near future - but perhaps they will occur in related, or even unrelated, areas, maybe driven by amazing progress in neuroscience, neuroimaging, optogenetics, etc.
Anon @06:13. I also believe there is something of a lull in MS research at the moment, al least in the area of neuroinflammation. The emergence of alemtuzumab and HSCT-BM as induction therapies and possible cures have turned the spotlight on repair (remyelinating agents and axonal regeneration). These areas include other neurodegenerative diseases.
Nice to see a positive view. Much appreciated
Getting ready for new HSCT results...excited
What do you mean MouseDoctor? Is there a new paper on HSCT coming out soon? Do you know roughly when (ie. next few weeks maybe)?
A bit of teasing MD?
You know me.....Dita von tease😎
http://www.nature.com/ncomms/2016/160426/ncomms11312/full/ncomms11312.htmlThe plot thickens in the understanding of astrogliotic scarring and axonal preservation/growth and remyelination. This report proposes that an inhibitor of CSPGs (found in gliotic scars) promotes remyelination. This inhibitor, 4-F-NAcGln stimulates remyelination by OPCs while the other drugs purported to promote myelination in vitro and in vivo(Clemastine and Benztropine) had minimal effect on demyelination in the presence of CSPGs inhibition. The astrogliotic scar preserves axons but a component of the scar is preventing demyelination?
I came across the link below with links Cerebral nocardiosis virus to Lemtrada. Not something I've heard of. The patient sadly died. Is it something to be worried about or a rare complication? http://www.medpagetoday.com/clinical-context/MultipleSclerosis/57171
Article about work of Prof. David Booth on EBV, vitamin D and MS in Australia.If you contract EBV before age 10 seems to have protection against MS, now you contract EBV and has IM after 20 years susceptibility to having MS it is 20 times higher...This comes Even? http://www.news.com.au/lifestyle/health/catching-glandular-fever-can-prevent-multiple-sclerosis/news-story/178db6f581478703c06090532f8c5c0d
There are some big news out, about how the inacurate regulation of NK-cells might contribute to the pathogenesis of multiple sclerosis. I am really looking forward to hearing from your opinion on this topic. For more details, see this publication:Catharina C. Gross, doi: 10.1073/pnas.1524924113Many greetings from Germany
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