Is Progressive Really different from RR MS

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Ratzer R, Søndergaard H, Christensen JR, Börnsen L, Borup R, Sørensen P, Sellebjerg F.Gene expression analysis of relapsing-remitting, primary progressive and secondary progressive multiple sclerosis.Mult Scler. 2013 Oct 1. [Epub ahead of print]

BACKGROUND:Previous studies of multiple sclerosis (MS) have indicated differences in the pathogenesis in relapsing-remitting (RRMS), secondary progressive (SPMS) and primary progressive (PPMS) disease.
OBJECTIVE:We hypothesized that different MS subtypes would show differences in gene expression that could be traced to specific subsets of peripheral blood mononuclear cells (PBMCs).
METHODS:Gene expression in RRMS, SPMS, PPMS and healthy control (HC) PBMCs was analyzed on Affymetrix arrays. In addition, we studied gene expression in pools of purified PBMC subsets.
RESULTS:We found 380 genes that were differentially expressed in RRMS, PPMS, SPMS and HCs (false discovery rate < 5%). There were no major differences between the subtypes of MS. The genes showing most prominent expression changes in RRMS were associated with adaptive immune pathways, while genes in PPMS were associated with innate immune system pathways. SPMS patients shared pathways with RRMS and PPMS patients. Gene expression changes were most prominent in B cells, CD8+ T cells and monocytes.
CONCLUSION: Differences in gene expression, which could be traced to B cells, CD8+ T cells and monocytes, were found between MS patients and HCs but only minor differences were observed between MS subgroups
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Histlogically there are similarities it is not surprising that there may be similar proteins expressed. However it shows inflammation in both. If Relapses are a problem of peripheral immunity looking in the brain yu may be monitoring progression

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  • On what I think is a related subject, as this research seem to be saying that there is only minor differences between sub-groups, is it possible that using DMD's can actually move you from RR to SPMS as a result of the law of unintended consequence. I am a Tysabri user and have not had a relapse for 3 years (hooray!), but can I really be considered as being relapsing remitting?.

  • A question related to the previous one.

    Does this study data indicate that Laquinimod, if it has neuroprotective effect in RRMS, will most likely have the same effect ( or more or less the same effect ) in SPMS and PPMS ?

    The LAQ data from ECTRIMS ( poster P1036 ) was especially interesting since it showed LAQ+non-relapsing VS Placebo+non-relapsing had very good data ( HR 0.611, p = 0.036, p value vs placebo )

    And from a logical point of view, at least for me, if RRMS, PPMS and SPMS are simular, a "proven effect" on non-relapsing MSers ( RRMSers ) indicate the drug candidate will have a simular effect on PPMSers and SPMSers.

    • I think that too.

      In my opinion the cause for MS will be found in ppMS. Relapses are caused by something different which has connection in some form to the "original" cause.
      Therefor the cause for relapses will be found in rrMS.

      They interact in some way or another but I think these are 2 seperate processes.

  • I try to re-post and hope for some feedback:

    Does this study data indicate that Laquinimod, if it has neuroprotective effect in RRMS, will most likely have the same effect ( or more or less the same effect ) in SPMS and PPMS ?

    The LAQ data from ECTRIMS ( poster P1036 ) was especially interesting since it showed LAQ+non-relapsing VS Placebo+non-relapsing had very good data ( HR 0.611, p = 0.036, p value vs placebo )

    And from a logical point of view, at least for me, if RRMS, PPMS and SPMS are simular, a "proven effect" on non-relapsing MSers ( RRMSers ) indicate the drug candidate will have a simular effect on PPMSers and SPMSers.

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