D’haeseleer et al. Vascular aspects of multiple sclerosis. Lancet Neurol. 2011 Jul;10(7):657-66.
This review claims that there are potentially three types of blood vessel or vascular abnormalities in MS:
(1) The study of diseases in the general population suggest that people with MS have a higher risk for stroke than people who do not have MS. The underlying mechanism of this unknown, but might involve damage to blood vessels secondary to brain inflammation that occurs in MS. Another proposed explanation is that MS’ers have a global reduction in blood flow to the brain.
“This is probably secondary phenomenon due to previous tissue damage as a result of MS. Whether this reduced blood flow predisposes MS’ers to stroke is not known.”
(2) Data suggest that a subtype of focal MS lesions might originate from reduced blood flow.
“This is very controversial and there is no consensus among card-carrying MS neuropathologists on this proposal.”
(3) CCSVI: the pathology of MS might be the consequence of a chronic state of impaired venous drainage from the CNS, for which the term chronic cerebrospinal venous insufficiency (CCSVI) has been coined. A number of recent studies do not support the CCSVI theory, but some elements of CCSVI might be explained by slower cerebral venous blood flow secondary to the reduced cerebral perfusion in people with MS compared with healthy individuals.
“I agree with the latter and would add the possible con-founder of dehydration, please see my previous post (click here).”
“On balance I don’t think the evidence is very strong that vascular abnormalities play a large role in MS. It is hard to explain a lot of what we know about MS with these vascular hypotheses or theories.”
CoI: Nil
Hot off the UK MS Society press:Researchers discover new approach that may repair MS damage27 Jun 2011Researchers part-funded by the MS Society have made a discovery that has the potential to lead to a drug treatment to repair damage caused by multiple sclerosis. They discovered a molecule that is capable of stimulating the body's own stem cells to repair myelin. There are currently no treatments that can repair the damage caused by MS. Researchers hope that this, as well as other discoveries, will lead to a treatment for people with MS within the next 10-15 years. What did the study show? The study focused on a specific set of stem cells in the brain that can turn into oligodendrocytes – which in turn go on to make myelin. The researchers found that when a protein called Axin 2 was present in the stem cells, they were able to convert into oligodendrocytes. But this protein can degrade within cells and is therefore not always present – and when missing, the stem cells could not develop into oligodendrocytes. The researchers needed to find a way of ensuring Axin 2 was present within these stem cells. They did this by using a molecule called XAV939 to stabilise the protein during tests in the lab. This was effective at ensuring the stem cells were able to convert into oligodendrocytes, offering hope that the molecule could lead to the development of a drug that replicates the effect in clinical trials. Dr Steve Fancy, lead author of the study said: "This work identifies Axin 2 as a molecule which seems to be important in myelin repair. Our hope is that we'll be able to use this knowledge to develop treatments that repair damage caused by MS." Moving towards a more effective treatment The work was published yesterday in the journal Nature Neuroscience. It was funded by the US and UK MS Societies and carried out by scientists at the University of California San Francisco and the University of Cambridge. The study was led by Dr David Rowitch of the UCSF Eli and Edyth Broad Centre for Stem Cell Research and Regenerative Medicine and Howard Hughes Medical Institute. Today's results follow ground-breaking research published last year from two of the MS Society's major investment centres, the Cambridge Centre for Myelin Repair and the Edinburgh Centre for Translational Research, which showed that targeting a different molecule promoted myelin repair in laboratory models of MS. This second discovery increases the likelihood that researchers will be able to tranlsate their findings into treatments that repair myelin in people with MS. Robin Franklin, Professor of Neuroscience at the University of Cambridge, who was co-author of the study said: "There are currently no treatments that repair myelin caused by MS, which is a missling link in the treatment of the condition. "This discovery means we now have even more credible opportunities to promote myelin repair, which is a really promising step forward. Our efforts will now be focused on translating these findings into treatments for people with MS." In April the MS Society committed a further £2.1 million over the next five years to Professor Franklin and his colleagues at the Cambridge Centre for Myelin Repair to continue his work. What does the MS Society say? Dr Doug Brown, head of biomedical research at the MS Society said "Myelin repair holds real potential to prevent or even reverse the devastating effects of MS. "We've made significant investment in myelin repair research in recent years and are delighted to see this starting to pay dividends. "We are excited to see this work moving towards clinical trials and are hopeful that this will lead to a new form of treatment for people with MS within the next 10-15 years."
Re Dr. Dre's commentThis news has been widely reported in the press today. The Independent- 27 June (Coverage also in The Times, The Telegraph, The Scotsman, The Herald, Press & Journal and The Sun)Dr Doug Brown of the MS Society is quoted in several of the above pieces of coverage. Simon Gillespie was also interviewed by Sky News Radio, and Dr Robin Frankiln was on this morning's Today programme.
You can hear Franklin's interview to BBC Radio 4 this morning by clicking on:http://www.bbc.co.uk/iplayer/b006qj9z/consoleSkip to the 46 minute point to hear his interview. Once again this treatment seems decades away but it's always nice to hear good news about MS treatments rather than the old news on assisted suicide etc.Prof G, maybe you should meet Franklin and exchange thoughts. Good idea or bad idea?
Re "Prof G, maybe you should meet Franklin and exchange thoughts. Good idea or bad idea?" Yes, we have met to discuss things and David Baker in group will be testing some of their strategies in our animal model (chronic relapsing EAE); that is if they get the programme funded of course.
Yeah, they may as well not even bother releasing press statements like this if treatments are so long away from being available to MS'ers.I mean come on! 15 years! Seriously? My disease has progressed at an unfathomable rate just in the last 5 years. I don’t think I’ll be alive in 15 years, or even worse, I’ll be beyond repair. It’s not fair. I’m 27 years old and have so little to go on in terms of hope.