Barking up the wrong tree


Have we got it all wrong. Peter stys from Canda gives his world view. As it is open source here you go click here


Maybe we can get him to explain his convolution

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  • I am also in favour of the inside-out model.
    I think that a degenerating process is in some form covered by the relapsing process.

    Which brings me back to my theory that the cause of MS (in this theory cytodegeneration) is differnt to the cause of relapses.

    • Thing is, why if you treat very early with a drug like Alemtuzumab, MS seems to be halted in it's tracks yet treatment later in the disease course still shows a degree of progression (nerve cell death).
      If the primary cause was nerve cell degeration, then this would be expected to continue regardless of whether the neuroinflammation inflammation has been stopped yet as mentioned above very early treatment seems to show the disease has indeed been halted (although obviously these MSers have to be followed up for many years to confirm this). So to my mind, it is the inflammation in the brain that is triggering a degenerative environment, which if allowed to proceed unchecked can over time lead to a situation where the nerve cell loss will continue irrespective of treatment of the neuroinflammatory response, indicating that neuroprotective strategies are needed at this stage.
      Our mouse studies would seem to confirm this scenario.

    • So going on from there, where does this fit with ppms ? and why no such treatments, what am I missing ? has the inflammation stage been and gone un-noticed ?

      Regards as always

    • Again, PPMS seems be primarily a neurodegenerative disease with not much inflammation (though I'm not sure what the microglial response is here, will look this up) and to lump it in with RRMS may have been a grave mistake that has held up research in this area for far too long. I think this is changing, with a focus on potential neuroprotective therapies.

    • As someone who was hospitalized with ADEM (Acute Dissemniated Encepholomyelitis) which is the most aggressive demylinating CNS disease, here are my thought on PPMS.

      In many cases of ADEM (including mine), MRI results may not show anything at initial presentation of symptoms. It has been suggested that MRI white matter activity follows recovery rather than decline.

      So if people with PPMS never relapse (no recovery) there may be little MRI activity.

  • @MD2 11:55:00 am

    Question: is Alemtuzumab fully understood?

    Maybe I am missing some information here. To my understanding, Alemtuzumab destroys B and T cells (specific to CD52). Are CD52 cells related to inflammation processes only?

    So if degeneration is a primary course, inflammation could be a road builder making it easier for the degeneration to spread.

    Nevertheless to my opinion it's the right way to stop or inhibit inflammation.

    And what about secondary progressive MS? To my understanding about 40% of the rrMSers devlop SPMS later in live no matter what.

    More data needed about the degenerating process taking place in ppl with rrMS?

    I think it will all become clearer once there are neuroprotective agents or even remyelinating agents availible.

    Spinng wheel got to got 'round 😉

  • Alemtuzumab binds to CD52, an antigen that is present on the surface of B and T lymphocytes, a majority of monocytes, macrophages, natural killer (NK) cells, and a subpopulation of granulocytes. So it depletes the majority of cells of the immune system. Over time these repopulate, with the time varying between subsets.

    And what about secondary progressive MS? To my understanding about 40% of the rrMSers devlop SPMS later in live no matter what.

    This data is based upon the old (not very effective) DMTs such as beta Interferon and Copaxone. I suspect with the new, much more effective at stopping relapses, DMTs the development of SPMS might be at least significantly delayed delayed if not completely abolished (as may be the case with early treatment with alemtuzumab..

    • I believe if natalizumab was used as a first-line treatment, as early as possible, progression would be greatly diminished. I also believe destruction of myelin is collateral damage due to activation of innate immunity. Pathogen as activator? "Bring in the usual suspects".

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