BG12 at ECTRIMS

Discuss Tecfidera (BG-12, dimethyl fumarate) as an oral treatment for multiple sclerosis.

BG12 at ECTRIMS

Postby patientx » Fri Oct 28, 2011 9:24 am

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Re: BG12 at ECTRIMS

Postby whyRwehere » Tue Nov 01, 2011 2:57 pm

Hmmm, a mold inhibitor that can cause serious allergic skin reactions....what's it doing on to the inside of the body??
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Re: BG12 at ECTRIMS

Postby NHE » Wed Nov 02, 2011 2:10 am

whyRwehere wrote:Hmmm, a mold inhibitor that can cause serious allergic skin reactions....what's it doing on to the inside of the body??


This post, and a few before it in the same thread, discusses some of the characteristics of dimethyl fumarate, e.g., chronic depletion of glutathione.

Biogen's investors seemed to have taken the news on the BG-12 studies in a positive light pushing the stock price up to $120/share recently. However, it will be interesting to see what the long term effects of this med are for the people taking it. For example, with depletion of glutathione, it might be the case that we see an increased sensitivity to things such as acetaminophen toxicity in the liver.

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Re: BG12 at ECTRIMS

Postby whyRwehere » Wed Nov 02, 2011 3:24 am

Thanks NHE, for the link. I think we'll pass on this. I predict that continual usage will not be kind to the human body, and then the stock price will fall. So, buy now and sell within the year. How sad.
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Re: BG12 at ECTRIMS

Postby NHE » Wed Feb 22, 2012 3:05 am

NHE wrote:This post, and a few before it in the same thread, discusses some of the characteristics of dimethyl fumarate, e.g., chronic depletion of glutathione.

Biogen's investors seemed to have taken the news on the BG-12 studies in a positive light pushing the stock price up to $120/share recently. However, it will be interesting to see what the long term effects of this med are for the people taking it. For example, with depletion of glutathione, it might be the case that we see an increased sensitivity to things such as acetaminophen toxicity in the liver.


Here's an interesting paper discussing the effects of glutathione depletion and its potential relevancy to ALS. What would Biogen have to say about this I wonder... Image

Depletion of reduced glutathione enhances motor neuron degeneration in vitro and in vivo.
Neuroscience. 2007 Feb 9;144(3):991-1003. Epub 2006 Dec 5.

    The mechanism of selective and age-dependent motor neuron degeneration in human amyotrophic lateral sclerosis (ALS) has not been defined and the role of glutathione (GSH) in association with motor neuron death remains largely unknown. A motor neuron-like cell culture system and a transgenic mouse model were used to study the effect of cellular GSH alteration on motor neuron cell death. Exposure of NSC34 motor neuron-like cells to ethacrynic acid (EA) or l-buthionine sulfoximine (BSO) dramatically reduced the cellular GSH levels, and was accompanied by increased production of reactive oxygen species (ROS) measured by the dichlorofluorescin (DCF) fluorescent oxidation assay. In addition, GSH depletion enhanced oxidative stress markers, AP-1 transcriptional activation, c-Jun, c-Fos and heme oxygenase-1 (HO-1) expression in NSC34 cells analyzed by a luciferase reporter, Western blotting and quantitative PCR assays respectively. Furthermore, depletion of GSH decreased mitochondrial function, facilitated apoptosis inducing factor (AIF) translocation, cytochrome c release, and caspase 3 activation, and consequently led to motor neuron-like cell apoptosis. In an ALS-like transgenic mouse model overexpressing mutant G93A-Cu, Zn-superoxide dismutase (SOD1) gene, we showed that the reduction of GSH in the spinal cord and motor neuron cells is correlated with AIF translocation, caspase 3 activation, and motor neuron degeneration during ALS-like disease onset and progression. Taken together, the in vitro and in vivo data presented in the current report demonstrated that decreased GSH promotes multiple apoptotic pathways contributing, at least partially, to motor neuron degeneration in ALS.

    The full paper is available at the above link

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Re: BG12 at ECTRIMS

Postby NHE » Wed Feb 22, 2012 3:15 am

Another cheerful paper discussing the effects of glutathione depletion, this time with relevancy to Parkinson's Disease.


Glutathione depletion and oxidative stress.
Parkinsonism Relat Disord. 2002 Sep;8(6):385-7.

    Oxidative stress is believed to contribute to the pathogenesis of Parkinson's disease. One of the indices of oxidative stress is the depletion of the antioxidant glutathione (GSH), which may occur early in the development of Parkinson's disease. To study the role of GSH depletion in the survival of dopamine neurons we treated mesencephalic cultures with the GSH synthesis inhibitor L-buthionine sulfoximine. Our studies have shown that the depletion of GSH causes a cascade of events, which ultimately may result in cell death. An early event following GSH depletion is a phospholipase A(2)-dependent release of arachidonic acid. Arachidonic acid can cause damage to the GSH-depleted cells through its metabolism by lipoxygenase. The generation of superoxide radicals during the metabolism of arachidonic acid is likely to play an important role in the toxic events that follow GSH depletion.


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Re: BG12 at ECTRIMS

Postby jimmylegs » Wed Feb 22, 2012 6:17 am

made me recall these:

general-discussion-f1/topic3800.html#p55853
"anyone else have another guess what handy nutrient elevates your glutathione???"

regimens-f22/topic2489-195.html#p138681
http://jn.nutrition.org/cgi/reprint/111/6/1098.pdf
Effect of Zinc Deficiency on Blood Glutathione Levels

general-discussion-f1/topic3800.html#p55856
(simpsons - 'jimmy wishes for a world without zinc')
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