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  • Grrrrrrrrrr! I'm not impressed with the NHS "Choose and Book" appointment system! An appointment that was booked for Barts neuro dept a month ago and due today was cancelled by a letter dated 6th November and delivered yesterday! I had to 'phone my GP to see if they knew why (they didn't – their letter has yet to arrive!) so I had to 'phone Barts. Apparently the cancellation reason was that the consultant I'd been allocated rejected me because my condition was not his speciality! As someone who works in systems and processes engineering, my opinion is that whoever designed / approved the system missed a HUGE piece of logic in the analysis, which causes frustration / upset / anger at the patient end and no doubt irritation at the doctor end. Thankfully a lovely lady in the appointments team at Barts is on the case to get me a new appointment with an MS consultant, but it was not a fun nor stress-free experience!

    • I agree the MO of a Troll or The Troll…maybe time to start writing to Leicester again.

      There is one easy way to save themselves from such feelings

  • Continued rant time!

    I called Barts today to see what was happening about rescheduling my appointment and was somewhat disappointed (!) to be told that this request was sitting in the inbox of the appointments department supervisor, because only he was able to select the right consultant for me to see! Said supervisor is away till Friday, so I will have to wait till then to call him, but for the love of all things holy, how can this be? There is a webpage for Barts that lists the neurology consultants and their specialties, and I have a diagnosis: how can someone other than the supervisor NOT be able to match me to a consultant? And why has this man of such great power been allowed to go away on leave without leaving a deputy? What if he gets hit by a bus?!

    Patience is apparently a virtue and I can only say I'm virtueless!

    • The Barancik Prize for Innovation in MS Research recognizes an exceptional scientist or TEAM whose work in MS research has demonstrated outstanding innovation and originality.

      If we don't get nominated we can't win anything. Is Team G innovate and original?…Yep but probably destined for US lab ********* springs to mind.

  • Prof G,

    When you have time I'd be greatful for a piece about neuro-protection therapies. I see that the MS Society (UK) is highlighting two trials on it's websie (amiloride and phenoine (?sp). Are there any others underway or planned? Any thoughts on what shows the most promise?


  • Are there any others underway or planned?


    The most promise…you have views but until studies are done and results are in you can never know.

  • I saw today in the DMSG (Deutsche Multiple Sklerose Gesellschaft) website, a news published yesterday from the University of Hamburg, in which they claim that blocking the Sodium channels (namely the TRPM4 channel) stops disease progression in EAE from mice, with a neuroprotective effect. They mention a drug used for Diabetes targeting the Na+ channel as well which is already in the market. I attach the link hereafter: http://www.dmsg.de/multiple-sklerose-news/index.php?w3pid=news&kategorie=forschung&anr=4534
    My question is: Now neuroprotection really seems like the main target for all of us (taking into account your multiple recent posts disregarding relapses as the main disability-driver), should we consider this approach while Phase III neuroprotective drugs are released?

    • I read it – yes, lots points to various channels, sodium or potassium. I think they are both somehow related. Interesting that they say that the disregulation of this sodium channel causes swelling of the nerve because it pumps too much water to compensate for too much sodium. However, even if they block the channel the inflammation (glial?) will continue – still I believe they are on the right track.

    • It depends on which cells express the channels many have channels on the glia and so drugs can have actions at this level as well as the nerve

    • The study has yet to be properly published, I do not know if they took blood samples for a pharmacokinetic/dynamic study. I think the neuroproective does is the symptom lowering dose or probably a bit less, based on animal studies.

    • Hi Andy,
      We did some work in this area that seems to be confirmed by this study back in 2005.
      Best wishes

      Chronic relapsing experimental allergic encephalomyelitis (CREAE) in plasminogen activator inhibitor-1 knockout mice: the effect of fibrinolysis during neuroinflammation.

      East E, Gverić D, Baker D, Pryce G, Lijnen HR, Cuzner ML.

      Neuropathol Appl Neurobiol. 2008 Apr;34(2):216-30

    • Ok, for the purposes of conversation let's say I've skipped through whilst eating a 'BLT' from Tesco (other Supermarkets are available.) on a lunch break.
      Does your paper deal with removing Fibrin removal as a therapy, but doesn't address why / how the Fibrin dpeosits form initially ? Or should I have had a longer lunch break?.
      I also have another paper along the same line (I Think ?), I would also appreciate your thoughts.


      Regards as always.

    • The paper shows that boosting the removal of fibrin (in this case by knocking out a gene that inhibits this) results in an improved disease outcome and less nerve damage. The fibrin deposits occur as fibrin leaks out from the circulation as the blood brain barrier is breached during an inflammatory attack.
      That was as far as we got as there was no money to take it any further.
      The recent report you quote seems to confirm our findings. I hope they cite our study!
      Hope this helps

    • Dear Andy
      Fibrinogen triggers astrocyte scar formation by promoting the availability of active TGF-beta after vascular damage.
      J Neurosci. 2010 Apr 28;30(17):5843-54.

      Indicates that fibrinogen injected into CNS causes astrogliosis, so with todays paper we get glia clustering also.

      Interesting question is what happens in Lewis rat EAE, there is essentially no demyelination or axon damage. I am not aware of any astrogliotic scar either, but the blood brain barrier is breached and presumably fibrinogen will get into brain.

      What gets the fibrinogen in in first place..T cells action on CNS:-)

    • Hi Andy,
      It's not rupture, it's the blood vessels of the microvasculature in the brain becoming leaky, allowing the entry of fibrin from the blood-stream. These blood vessels are normally very tightly sealed to stop any nasties getting into the CNS. Once the inflammation is resolved the blood vessels tend to re-seal which is analogous to gadolinium enhanced lesions fading in MS patients shown by MRI.
      It looks like the fibrin deposition can activate resident immune cells in the brain called microglia to clear the fibrin but when activated they can release chemicals which are neurotoxic.
      Activated microglia are implicated in the pathology of Alzheimer's and may be the cells responsible for the damage seen there.

    • If vessels were rupturing we would see it in the histology of MS and you would expect red blood cells in the brain. EAE in rhesus monkies is haemorrhagic and is unlike MS. In rodents I know they do not rupture in lesions as I have seen inside the blood vessels using scanning electron microscopy.

      The picture in the post tomorrow is misleading as it implies the junctions in the blood vessels have gaps in them they don't.

  • Spiegel online in Germany recently published an article about Glibenclamid that seems to have promising effects on MS. Could you let me have your views on this diabetes medication?
    "Im Tierversuch zeigte ein Diabetes-Medikament Wirkung gegen die chronische Krankheit Multiple Sklerose. Es hemmt zwar nicht die Dauerentzündung, die an Nervenzellen entsteht, schützt aber die Neuronen vor deren Folgen. Die Forscher hoffen, dass die Erkenntnis bald Kranken hilft" (Spiegel online, 19 November 2012).

    Thank you

  • Are we any closer to figuring out know what the oligoclonal bands bind to? What has been excluded so far? What is the likely target – axons, glial cells, intra-cellular components released into CSF after cell damage has occured? Are they the cause or the consequence of disease?

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