Research Day Talk: Early MS lesions

Today is DoctorLove telling about early MS lesions. 

DoctorLove’s Beau, Hans, or Doctor CryAb was going to talk about his trial on treating autoimmuntiy with alpha B crystallin and how EBV can trigger the autoimmune target, but because of talking about forest fires, there was not enough time. He turned up for questions, which we did not film. There will always next time.

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  • EBV-> sequence motif RRPFF -> traines the immunesystem
    alpha-B-crystallin -> sequence motif RRPFF -> triggers the immunsystem

    Alpha-B-crystallin can also be triggered by heat and stress. So this could also explain Uthoff. AND it could explain why relapses are closly related to times of stress.

    But this is nothing new and around for over 20 years. In fact I know that this theory is discussed on some boards on the internet. The guy who came up with this idea published over 50 pages of data (still! ongoing) and wants to start a privately funded study for a treatment incl. all normal and state of the art methods used up to day. Incl. MRI scans etc. pp.

    Completly financed by private money! No Pharma involved!
    It will be a single blinded (as it seems not to be possible to set up a double blinded study), placebo controlled study. Starting 2014/2015. There will also be a call on some crowd funding pages.

    Just in case you might not heard of this.

  • If pre-active lesions occur in healthy people, what stops the T-cells from crossing the blood brain barrier when they are signaled from the macrophages?
    If this new therapy is to shut-down the permeability of the blood brain barrier it seems like it would be no different than the already developed drugs that have the same purpose.

  • I'm not able to view the video but would like to ask a question about MRI and lesions. As MRI is the main tool to monitor progression and response to drug trials in RRMS how useful and accurate is it in monitoring progression /diagnosis in PPMS. Given that people who have PPMS tend to be older how do you distinguish between MS lesions and normal ageing? The reason I ask is that I have a positive lumber puncture, positive objective clinical signs, progressive weakness of the legs and arms but MRI shows only tiny T2W and Flair hyperintense foci scattered in white matter of both cerebral hemispheres including the per ventricular. Despite continuous progression the findings on MRI seem to puzzle everyone. Can you really attribute the findings which also include some atrophy of the brain, to ageing to someone in their late 40,s. who has significant disability? Any ideas from the team would be gratefully received.

  • It seems that the premise is that high local production of alpha B-crystallin by oligodendrocytes occurs in people with MS and that this is the key to stopping lesion formation.

    In essence, this is a defect of the oligodendrocytes. But if this is the case, then why do people who undergo HSCT regimens such as that performed by Dr. Richard Burt at Northwestern go into long lasting remision if it is undertaken early in the RRMS course of the disease? HSCT resets the immune systems, not oligodendrocytes.

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