Multiple Sclerosis (MS) Support Group
This community is a place where members can discuss current events and weigh in on what's going on in the world.
Usually docs want at least 2 complete trials with conclusions before they will prescribe for you. If all the current meds are not working which means you are a more likely need to try something new to TRY to help you.
Riluzole is well established at reducing glutamate in ALS and is one of there best drugs against this disease. See following on how ALS is like MS including high glutamate which is the target of this drug Riluzole. http://www.jneuroinflammation.com/content/9/1/20
NIH research of Riluzole on MS all seems positive.
1.) http://www.ncbi.nlm.nih.gov/pubmed/15949499
Extracellular accumulation of glutamate contributes to excitotoxic injury of neurons and glial cells, suggesting that the maintenance of subtoxic extracellular glutamate levels may be crucial. Riluzole is a neuroprotective agent that inhibits the release of glutamate from nerve terminals and modulates glutamate, i.e., kainate and NMDA receptors. It inhibits excitotoxic injury in several experimental models of neurodegenerative disease. We performed a small run-in versus treatment MR-monitored pilot study in 16 primary progressive MS patients. The results suggest that riluzole reduces the rate of cervical cord atrophy and the development of T1 hypointense lesions on magnetic resonance imaging in primary progressive MS. The rate of brain atrophy was only slightly decreased. The results indicate an effect on mechanisms involving lesion evolution and axonal loss, but no clear effect on new lesion formation. However, the data suffer from several limitations and must be confirmed in future trials.
2.) http://www.ncbi.nlm.nih.gov/pubmed/14556941
In conclusion, our study demonstrates, for the first time, that riluzole can reduce inflammation, demyelination and axonal damage in the CNS and attenuate the clinical severity of MOG-induced EAE. These results suggest that riluzole, a drug used in amyotrophic lateral sclerosis (ALS), might be beneficial for the treatment of MS.
http://clinicaltrials.gov/ct2/show/NCT00202397
Phase 2 trial done
Best wishes to all,
EP
Riluzole is well established at reducing glutamate in ALS and is one of there best drugs against this disease. See following on how ALS is like MS including high glutamate which is the target of this drug Riluzole. http://www.jneuroinflammation.com/content/9/1/20
NIH research of Riluzole on MS all seems positive.
1.) http://www.ncbi.nlm.nih.gov/pubmed/15949499
Extracellular accumulation of glutamate contributes to excitotoxic injury of neurons and glial cells, suggesting that the maintenance of subtoxic extracellular glutamate levels may be crucial. Riluzole is a neuroprotective agent that inhibits the release of glutamate from nerve terminals and modulates glutamate, i.e., kainate and NMDA receptors. It inhibits excitotoxic injury in several experimental models of neurodegenerative disease. We performed a small run-in versus treatment MR-monitored pilot study in 16 primary progressive MS patients. The results suggest that riluzole reduces the rate of cervical cord atrophy and the development of T1 hypointense lesions on magnetic resonance imaging in primary progressive MS. The rate of brain atrophy was only slightly decreased. The results indicate an effect on mechanisms involving lesion evolution and axonal loss, but no clear effect on new lesion formation. However, the data suffer from several limitations and must be confirmed in future trials.
2.) http://www.ncbi.nlm.nih.gov/pubmed/14556941
In conclusion, our study demonstrates, for the first time, that riluzole can reduce inflammation, demyelination and axonal damage in the CNS and attenuate the clinical severity of MOG-induced EAE. These results suggest that riluzole, a drug used in amyotrophic lateral sclerosis (ALS), might be beneficial for the treatment of MS.
http://clinicaltrials.gov/ct2/show/NCT00202397
Phase 2 trial done
Best wishes to all,
EP
Example info would be useful:
Can you take this drug with existing CRAB (immune modulator) drugs
How long before you see results, etc
General comments from someone who has taken the drug
I will say I do like that fact that is well established safety in another disease already. It is just ALS is more progressive than MS. The main target excess glutamate is in both diseases.
So again if anyone has more info (was involved with the clinical tirals) please post positive or negative info I would just like more information as this looks promising (not a cure but slowing of symptoms).
Best wishes,
EP
Well amino acids are needed for immune system and the brains of those with MS have very high glutamate as in ALS.
So how is reducing glutamate going to help?
Well what can excess glutamate do to your brain?
Excess glutamate is thought to be damaging nerves in both these diseases because of constant neuro-stimulation without calming GABA like normal brain. Plus because glutamate is in excess, not at healthy level, it interferes with mitochondrial function that reduces ATP. This lack of fuel (ATP) is thought to be contributing to the inability to repair thus contributing to nerve damage too.
"any port in the storm" I told my hubby he better not "port" anywhere but with ME. *thunder of laughter" As my grandma used to say "It is alright to window shop as long as you bring your appetite home." I am a firm believer in that statement.
Yes please post any info you have or can obtain on BG-12 and Riluzole.
I have a special post in my subgroup below where I have some info on both of these drugs (see page two)
http://www.dailystrength.org/groups/loved-ones-who-support-someone-with-ms/discussions/messages/13042864
Thanks,
EP
You know that photo I uploaded for you to see a few days ago, the one of the diagram I made with the amino acids. This is actually what I am looking at, so it is intriguing. I think there are a few other strategic methods of therapy that could also help along these lines...but this will take quite some time to look at in research.
This drug though has been used for years with ALS. So it has had test runs already...kinda like LDN has been used for decades without huge negative side effects. I always feel safer with these kinds of meds. Anywho.
Best wishes to all,
EP
So could you have serum glutamate checked every 2 months then when you see it elevate take this Riluzole to reduce the glutamate & try to prevent relapse? Good question to ask your doctor with the below research and above links printed out and in your hand while you discuss your options.
________________________________
http://www.sciencedirect.com/science/article/pii/0022510X8090088X
Abnormal glutamic acid metabolism in multiple sclerosis
Fred C. WestallCorresponding author contact information,
Angela Hawkinsa, George W. Ellisona, Lawrence W. Myers
Abstract
"We have found extensive amino acid abnormalities in multiple sclerosis sera. The most consistent abnormality is an elevation in serum glutamate, which is most striking during relapses. The increase in glutamate in the patients does not occur sharply during the onset of the relapse. Instead it appears to rise gradually within a month or two prior to the onset of the clinical relapse, to reach a peak during the relapse and then to slowly decline."
http://www.scribd.com/doc/90242205/A-case-of-multiple-sclerosis-improvement-following-removal-of-heavy-metal-intoxication
http://www.matteodallosso.org/eng/
http://www.dailystrength.org/c/Multiple_Sclerosis_MS/forum/14124635-great-news-ms-patients
I agree heavy metals can mimic MS just like Lymes, ALS, Lupus, B vitamins deficiency, etc. I don't think heavy metals cause MS in the majority of people that have MS, but might be root cause for a small subset. I DO think that if you have too much heavy metals in your system that they can contribute to symptoms (Aluminum is a known neurological damaging metal as is Mercury, etc). Chelation may help reduce symptoms if your levels are elevated.
Glutamate is high in the brains of those with MS and high in the blood before onset of a relapse. So reducing these levels may help slow disease by putting glutamate at healthier level THUS decreasing un-needed extra neuro-stimulation and getting more ATP from Mitochondria.
I am keeping my eye on this,
EP
Here's another thing you might be interested in. It might not be there for long so if you are at all interested you might want to download.
http://www.scribd.com/doc/90525850/Gd-Induced-Oxidative-Stress-Triggers
The link is kind of garbled but it looks like the info below (title might be a bit different as I said link is garbled). Journal of Neurochemistry (2011) 117, 38-47. Title Gadolinium (dye used in MRIs) induced Oxidative stress triggered in endoplasmic reticulum stress in rat cortical neuro. by Qing Xia, Haifeng Haung, Lingyan Du
If anyone is interested they can do a google search on this article.
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Gast,
I think you misunderstand me. Yes I think this is a good info for many people with MS because more might get Chelation therapy to reduce symptoms and for a lucky FEW they might get rid of their symptoms.
HOWEVER, I do not like to give false hope but rather helpful info that could reduce symptoms. I am being cautiously optimistic. I know that first year my hubby latched on to ideas like this one on the thinking he had something else and it fed his denial. Worse he was very depressed when they did not work for him. He did have heavy metals checked (not high) and had fillings taken out (see URL in reply #12 where I also say I am happy this info is getting out to hopefully reduce symptoms). Neither improved his symptoms..I think it might for some who have high levels. YES get it checked just like ruling out Lupus, RA, Lymes etc. (Like I said at beginning of reply12). Just because I do not tote it to be a cure all does not mean I don't think may contribute to some the neurological symptoms in those people with MS AND heavy metal excess.
Best wishes,
EP
My gadolinium levels were at toxic levels four years after exposure but the mercury and lead didn't show up until after exposure. I've had three urine metals testing done and two were provoked.
I understand your concern...I sometimes think I can save everyone but I can't LOL! I just have to take care of myself. I wonder why that link didn't work. Here's the abstract:
Gadolinium-induced oxidative stress triggers endoplasmic reticulum stress in rat cortical neurons.
J Neurochem. 2011 Apr;117(1):38-47. doi: 10.1111/j.1471-4159.2010.07162.x. Epub 2011 Feb 11.
Xia Q, Feng X, Huang H, Du L, Yang X, Wang K.
Source
State Key Laboratory of Natural and Biomimetic Drugs and Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing, China. xqing@bjmu.edu.cn
Abstract
Introduction of Gadolinium (Gd) to the nervous system is linked to the development of neurotoxicity involving both oxidative and endoplasmic reticulum (ER) stress. Gd levels (0.2-20 m) in the form of gadolinium trichloride (GdCl(3)) cause neurotoxicity in vitro. We investigated the signaling pathways in primary cultured rat cortical neurons and tested whether GdCl(3) induced oxidative and ER stress. Results showed that Gd-induced neural cell death followed a rapid accumulation of intracellular reactive oxygen species. In addition, Gd exposure resulted in spliced X-box binding protein 1 mRNA and increased expression of binding immunoglobulin protein, thus activating transcription factor 4 (ATF4), ATF6, and C/EBP homologous protein mRNA. Up-regulated expression of binding immunoglobulin protein is a hallmark of ER stress and C/EBP homologous protein is an ER stress-related pro-apoptotic transcription factor. Activation of ER stress downstream substrates, inositol-requiring kinase 1 and ATF6, was also observed in Gd-treated cells. The neurotoxic effects of Gd were blocked by the antioxidant N-acetylcysteine. Results demonstrated that Gd-induced cytotoxicity in neurons occurs via oxidative injury and ER stress-related signal transduction, thus offering new insight into the neurotoxicology of gadolinium.
2011 The Authors. Journal of Neurochemistry 2011 International Society for Neurochemistry.
PMID:
21198628
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/21198628