caution larry

Hi, I’m Kim! This site provides a little insight to my journey of being diagnosised with Remitting Relapsing Multiple Sclerosis on October 26th 2004. I review books and documentaries, post MS-related news, and share my photos.

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Wednesday, April 11, 2007
Modified Bone Marrow in mice MS (EAE)

2007-04-11 14:02:28

Interesting findings posted
showing this treatment reduces nerve damage and stopped myelin loss in mice
with the mouse version of MS: "Harald Neumann and his colleagues realised that
bone marrow cells called myeloid
precursor cells
could be the answer because they naturally migrate into
the CNS and can form microglia, which act as immune cells for the CNS and could
clear the debris. Microglia also produce a protein called trigger receptor expressed
on myeloid cells-2 (TREM2). The scientists collected myeloid precursor cells
from mouse bone marrow and modified it to produce TREM2. These cells were then
injected into mice with experimental autoimmune encephalomyelitis (EAE), which
is used as an animal model for MS. Normal myeloid precursor cells were also
injected as a control. In healthy mice or those only just beginning to show
symptoms of EAE, neither cell type migrated to the spinal cord. However, when
EAE symptoms were at their peak, both sets of myeloid precursor cells migrated
into the mice' spinal cords where the TREM2-producing cells reduced nerve damage
and halted myelin loss. The therapeutic cells also increased the amount of debris
cleared, and an anti-inflammatory environment was created. This was shown by
increased levels of interleukin-10 (IL-10), a human cytokine that prevents the
production of pro-inflammatory cytokines such as pro-inflammatory cytokines
like Interferon-gamma, IL-2, IL-3, TNF-alpha and GM-CSF. However, in an article
detailing the results in PLoS
the researchers admit that although increased IL-10 levels might
be due to the TREM2-modified cells, "we cannot exclude the possibility
that TREM2-transduced myeloid precursors act indirectly via a secondary immune
organ to stimulate a regulatory immune cell type migrating into the CNS".

The authors go on to explain that IL-10 helps regulate the immune system and
is vital for the recovery phase of EAE; remission has been shown to be impaired
in IL-10-deficient mice (as previously
by scientists at Harvard Medical School). "TREM2-transduced
myeloid precursor cells applied intravenously ameliorate EAE either locally
inside the CNS or indirectly via another regulatory
immune cell type
by clearance of tissue debris and resolution of inflammation, thereby opening
new avenues for cell therapy of inflammatory and degenerative CNS diseases,"

the authors conclude."

Which MS drug (CRA or B) costs less over time?

2007-04-11 14:09:20

big study
just came out showing that Copaxone is the big winner at being
cheaper over time in managing MS symptoms. This type of info concerns me at
bit... in that insurance companies will use this to dictate what form of treatment
you should be on instead of what your doctor feels you should be doing for your
disease. If you're prescribed something different that agrees with you more,
will you not get coverage based on the assumed costs to the insurance folk?
Ugh. "A literature-based Markov model was developed to estimate the economic
outcomes of five treatment strategies: symptom management (e.g., physical therapy/exercise
and pharmacological treatment) alone and symptom management combined with COPAXONE®
(glatiramer acetate injection), IM-IFNβ1-a
(Avonex®), SC-IFNβ1-a
(Rebif®), or SC-IFNβ1-b
(Betaseron®) in patients
diagnosed with RRMS. This is the first economic model in MS to incorporate long-term
data on treatment effects, account for differences among clinical trial designs
of the immunomodulatory therapies and present the results in terms of cost-utility
and cost-effectiveness. The model design took into account disease modifying
therapy (DMT) acquisition costs, state-specific MS-related medical costs and
the cost of lost worker productivity. The analysis found that the total cost
per patient over the time horizon of a patient's
lifetime for COPAXONE® was
estimated to be 34.7 percent, 16.8 percent and 14.5 percent less than Rebif®,
Betaseron® and Avonex®,
respectively. Sensitivity analyses showed the results to be sensitive to changes
in health state utilities, the percentage reduction in disease progression rates
as measured by EDSS in the first two years of therapy used to estimate immunomodulatory
therapy treatment effects, model time horizon and immunomodulatory therapy acquisition