Thursday, 31 October 2013

Shift MS reports

You may have seen clips of Team G and other members fron UCLP in the MS reports by Shift MS



Here is the full interview of Prof B talking to Mariam
and then Prof G...as you can see the minute per answer (look at the egg-timer) just wasn't going to happen.

NB. International Collaborative has been rebranded as the MS Alliance

View it bit by bit

6 comments:

  1. Although I believe EBV or HERV's are most likely the trigger for MS in genetically suseptible people, but I do not believe they are the cause of the disease.

    I think this is vastly different than saying that they are the direct cause of MS, meaning they are directly responsible for the damage that occurs in the disease. To me, this is highly unlikely because nearly all humans have these viruses and because of this, MS should be more common but it isn't. Most people with these viruses have no ill effect, so I don't think they are the direct cause of MS.

    So, why do you think the opposite? The vast, vast, vast majority of data indicates that MS is an autoimune disease. Likewiese, there is overwheliming data that global warming is real and caused by man-made emisons of green house gasses. But there is a small minority of scientist who believe global warming isn't real and claim it is an umproven phenomenon and the cause is not known which unfortunately gets perpetuatedd as the state of the debate.

    So, I would put you in the later category where you are a small minority of scientists who believe MS is not an autoimmune disease.

    If you can point to some specific data that supports your theory, I would appreciate it. Maybe you can change my mind.

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    Replies
    1. The issue of a viral aetiology is too important to discard. The evidence against MS being autoimmune is voluminous; simply too much to comment on in a response. If MS is autoimmune can you please tell what the autoantigen is? In the earliest lesions identified (Barnett and Prineas lesion) there is massive death of oligodendrocytes by apoptosis without an inflammatory infiltrate. Why?

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    2. I think the best evidence for autoimmunity is disease worsening in the failed altered peptide ligand studies where exacerbations occurred. However, some of the people in the study developed a disease of the peripheral nervous system (not ms)

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    3. Maybe you should focus some of your attention and resources to the KIR4.1 autoantibody recently discovered in a large percentage of MSers :

      http://www.frontiersin.org/Journal/10.3389/fneur.2013.00125/full

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    4. The paper on C. perfringens is important not necessarily for causation but for addressing the importance of BBB integrity and MS. This is an important initial event in the pathology. After BBB is disrupted the cascade of CNS inflammation ensues. I agree with Dr. G. Where is the autoantigen? Why is there apoptosis of oligos preceding inflammatory cell infiltrate? Study at UCSF http://www.ncbi.nlm.nih.gov/pubmed/23187627 Microglia are activated due to BBB permeability and fibrinogen entry. HIV tat protein leads to BBB compromise as well as ETX in C. perfringens.

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    5. The pre-active lesions with microglial activation are not typically associated with blood vessels and I wonder if there is really local blood brain barrier breakdown. This could suggest that the toxin is not activating the blood vessels through which it should pass and then activate the microglia. Can this be worked into the idea?

      The infiltrate or single cells can produce factors that promote damage.

      The possibilities are quite great

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