Chaz wrote:I consider myself to be fairly bright, did ok on the SATS, did well in college and so on...
When Brian was diagnosed with MS this year I became the "researcher". I've looked into everything. Investigated all the treatment options, looked into new diets, asked for help in determining good vitamins and other supplements, but I just can't wrap my mind around the treatment studies. I get lost with the numbers and confusing statistics.
I wish there was a completely unbiased, easy-to-read report that laid the facts out plain and simple!!! I feel confident with the decision to go on Copaxone...it SEEMS like the best option for him and he has handled the daily injections well with little to no side-effects, but what is the real story behind this drug? What are the "simpleton" stats?!?! I know that nothing surrounding this disease is a definite, but I'd like to really understand Copaxone. I understand that it mimics myelin and I've seen some reports that say it may slow down progression (or relapse rates) by 30% but I don't know if I even have that right!
I don't know how unbiased this article is, if my memory serves me correctly, R. Arnon was one of the initial developers of copaxone. Anyways, in light of the potential bias, here's an article which discusses copaxone's method of action.
Mechanism of action of glatiramer acetate in multiple sclerosis and its potential for the development of new applications.
Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14593-8.
Glatiramer acetate (GA, Copaxone, Copolymer 1) is an approved drug for the treatment of multiple sclerosis and is highly effective in the suppression of experimental autoimmune encephalomyelitis in various species. The mode of action of GA is by initial strong promiscuous binding to MHC molecules and consequent competition with various myelin antigens for their presentation to T cells. A further aspect of its action is potent induction of specific suppressor cells of the T helper 2 (Th2) type that migrate to the brain and lead to in situ bystander suppression. Furthermore, the GA-specific cells in the brain express the antiinflammatory cytokines IL-10 and transforming growth factor beta, in addition to brain-derived neurotrophic factor, whereas they do not express IFN-gamma. Based on this immunomodulatory mode of action, we explored the potential of GA for two other applications: prevention of graft rejection and amelioration of inflammatory bowel diseases. GA was effective in amelioration of graft rejection in two systems by prolongation of skin graft survival and inhibition of functional deterioration of thyroid grafts, across minor and major histocompatibility barriers. In all transplantation systems GA treatment inhibited the detrimental secretion of Th1 inflammatory cytokines and induced beneficial Th2/3 antiinflammatory response. GA was effective also in combination with low-dose immunosuppressive drugs. Inflammatory bowel diseases are characterized by detrimental imbalanced proinflammatory immune reactivity in the gut. GA significantly suppressed the various manifestations of trinitrobenzene sulfonic acid-induced colitis, including mortality, weight loss, and macroscopic and microscopic colonic damage. GA suppressed local lymphocyte proliferations and tumor necrosis factor alpha detrimental secretion but induced transforming growth factor beta, thus confirming the involvement of Th1 to Th2 shift in GA mode of action.
Here's another article...
Glatiramer acetate: mechanisms of action in multiple sclerosis.
Int Rev Neurobiol. 2007;79:537-70.
Glatiramer acetate (GA), formerly known as copolymer 1, is a mixture of synthetic polypeptides composed of four amino acids resembling the myelin basic protein (MSP). GA has been shown to be highly effective in preventing and suppressing experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). Therefore, it was tested in several clinical studies and so approved for the immunomodulatory treatment of relapsing-type MS. In contrast to other immunomodulatory MS therapies, GA has a distinct mechanism of action: GA demonstrates an initial strong promiscuous binding to major histocompatibility complex molecules and consequent competition with various (myelin) antigens for their presentation to T cells. In addition, antigen-based therapy generating a GA-specific immune response seems to be the prerequisite for GA therapy. GA treatment induces an in vivo change of the frequency, cytokine secretion pattern and the effector function of GA-specific CD4+ and CD8+ T cells, probably by affecting the properties of antigen-presenting cells such as monocytes and dendritic cells. As demonstrated extensively in animal experiments, GA-specific, mostly, T helper 2 cells migrate to the brain and lead to in situ bystander suppression of the inflammatory process in the brain. Furthermore, GA-specific cells in the brain express neurotrophic factors like the brain-derived neurotrophic factor (BDNF) in addition to anti-inflammatory T helper 2-like cytokines. This might help tip the balance in favor of more beneficial influences because there is a complex interplay between detrimental and beneficial factors and mediators in the inflammatory milieu of MS lesions.