potential mechanism for transition to secondary progressive

[Cece]

http://link.springer.com/article/10.100 ... -8?LI=true

A shift from adaptive to innate immunity: a potential mechanism of disease progression in multiple sclerosis

Howard L. Weiner

Abstract
Multiple sclerosis is postulated to be a T cell-mediated autoimmune disease characterised by a relapsing-remitting stage followed by a secondary progressive phase. The relapsing remitting phase may involve waves of proinflammatory Th1 and Th17 cells that infiltrate the nervous system, provoking a clinical attack. The activity of these cells is modulated by other populations of regulatory T cells and the balance between the pro-inflammatory and regulatory T cells is critical for determining disease activity. Promoting the activity of regulatory cells is a potentially beneficial therapeutic strategy, and probably contributes to the action of glatiramer acetate. The progressive phase of multiple sclerosis is believed to be secondary to neurodegenerative changes triggered by inflammation. The status of the innate immune system and its relationship to the stages of multiple sclerosis has been poorly defined until recently. However, recent data suggest that these results demonstrate abnormalities of dendritic cell activation or maturation may underlie the transition to the progressive phase of the disease. Preventing this transition, perhaps by acting at the level of the innate immune system, is an important treatment goal. The identification of biomarkers to predict disease course and treatment response is a major challenge in multiple sclerosis research. Studies using antigen arrays have identified antibody patterns related to CNS antigens and heat-shock proteins that are associated with different disease stages and with response to therapy. In the future, such antibody repertoires could be used as biomarkers for the diagnosis and evaluation of patients with multiple sclerosis, for matching treatments to individual patients and, potentially, to identify healthy individuals at risk for this autoimmune disease.

Abnormalities of dendritic cell activation or maturation may be responsible for the shift from RR to SP?
Maybe some research could be done on how to prevent this shift. Even Big Pharma would benefit from all the patients who could stay RR and continue taking drugs.
I am RR right now and don't want to ever go SP *knock on wood, say a prayer*.

[CureOrBust]

I am RR right now and don't want to ever go SP *knock on wood, say a prayer*.

Severely off topic, but your statement caught my interest. I thought your CCSVI treatment was very effective against your MS symptoms, so was surprised to see you define yourself as RR. Have you had relapses of recent? or are you simply suffering residual effects from your MS? (PS: to counteract taking your thread off topic, I have bruised my knuckles for you knocking on my table )

[Leonard]

the answer is here:
http://www.ncbi.nlm.nih.gov/pubmed/22736750

this thread puts things in context:
http://www.thisisms.com/forum/general-d ... 15188.html

[Cece]

I am RR right now and don't want to ever go SP *knock on wood, say a prayer*.

Severely off topic, but your statement caught my interest. I thought your CCSVI treatment was very effective against your MS symptoms, so was surprised to see you define yourself as RR. Have you had relapses of recent? or are you simply suffering residual effects from your MS? (PS: to counteract taking your thread off topic, I have bruised my knuckles for you knocking on my table )

Well my last relapse was June 2010, which was before my first CCSVI procedure, so that's to the good. But that was also my only relapse since getting diagnosed in January 2006, which was 4 1/2 years before that. It's been 2 years since my CCSVI procedure but my relapses are rare enough that that's not unexpected to go that long without having a new relapse. I also am aware that I had 35 years of living with nearly fully obstructed jugulars: what has that done to my brain?

But yeah my vision is amazing, mild foot drop gone, fatigue vastly improved, cogfog vastly improved. Appetite and sense of taste still amazing, bladder is good. Numbness is gone.

From my three years now of engagement with the CCSVI concepts, I think CCSVI and MS are entwined diseases but not identical. As long as my veins are clear, I may never go back to that state of painful fatigue and cogfog that I was in, if those were a result of reduced blood flow due to CCSVI. But if there is degeneration that has been set in motion with the MS, that might continue even though the CCSVI is treated.

Bruised knuckles, lol!