This Is MS Multiple Sclerosis Knowledge & Support Community

Dear all,

The Boston Cure Project site has posted an article today about Tovaxin - a T Cell vaccine. An individual provides details of his success with this treatment. Does anyone have any more information on this treatment - looks promising?

Bromley


http://www.bostoncure.org:8080/article. ... ode=nested


It's interesting how those treatments which stop attacks (Campath and Tovaxin), rather than just reduce attacks (the CRAB drugs only reduce the attacks by 30%ish) appear to allow the body to start some repairr work. It does also seem to indicate that ms is an auto-immune disease (or is in some cases of ms).

Hello Bromley,

Interesting, but has anyone thought about the fact that if MS is caused by an infection, no matter how much you play about with the t-cells, the pathogen is still there and left untreated there are two possibilities: you might be lucky and manage to clear it from your system, which is a possibility because it has happened someone in the placebo arm of the last CPn trial at Vanderbilt. On the other hand, the pathogen might run amok and cause all kinds of havoc, which is maybe why campath proved singularly unsuccessful with people with SPMS, on whom it was first trialed. It seemed to work for a while and then the disease restarted its progression. I can't post any links about this because it is just my theory, but the fact remains that I, with early SPMS, got better on antibiotics, not anything else. I have improved as much as anyone that I have read about on any of the campath trials, say.

Sarah

Anecdote,

Yes - you're right these treatments only seemed to have some benefits at the early stage of the disease - but they may stop the disease progressing to SPMS (only time will tell). I think you are the only case of someone with SPMS who has shown that the damage can be reversed and this is due to the treatment you are receiving.

All the best.

Bromley.

Bromley,

You just caught me before going for some food. No, I'm not the only one, just the only one who has posted here. If you have been progressive for too long, and by this I mean quite a long period, because I had been progressive for about three years, even antibiotics don't seem to work. I was just caught in time, thank goodness.

Take care,

Sarah

This really does sound encouraging. I admit to not having an in-depth understanding of all the various drugs in clinical trials, but I'm wondering if the mode of action of Tovaxin isn't similar enough to Tysabri that the same PML problem might be a risk with the Tovaxin as well. Or am I just completely misinformed?

bromley wrote:Anecdote,

(...) I think you are the only case of someone with SPMS who has shown that the damage can be reversed and this is due to the treatment you are receiving.

All the best.

Bromley.

Some treatments cause improvements also in individuals with SPMS. The most important case (my opinion) is Novantrone. It stops progression for some SPMS patients and even seems to reverse it for some other SPMS patients; on the other hand, seem to have no impact on progression on other patiens.
It is not rare in many MS forums to hear about SPMS patiens able to achieve an improvement in their EDSS thanks to Novantrone treatment. This improvement is limited in time due to the long term toxicity.

Hope it helps.

Riccardo

The improvement discussion brings up what I have known about my husband all along. He is RRMS. Even in his early days of DX, up to 24 hours before an attack, he would have significant improvement in old symtoms. Sometimes to the point of seeing with a otherwise totally blind eye. No light, no nothing. All of a sudden he began to see light and forms. If his blindness is due to scarred nerves, then how can it get better? He drags his right leg. Once it started walking normal for a couple of hours. Within 24 hours, he had a lower extremity attack. Which leads me to believe that if there was something that could put the diease "at rest", then there would be a noticable improvement on the Disability Scale. For him, anyway. And yes this is just my theories and hind sight.

"I can't post any links about this because it is just my theory, but the fact remains that I, with early SPMS, got better on antibiotics, not anything else."

Hi to all,

Here are two abstracts about an antibiotic (Minocycline) used for MS.

Best regards, Tim

Reported June 4, 2004
Acne Drug Treats Multiple Sclerosis
A drug currently used to treat conditions including acne has been found to decrease the lesions in the brains of people with multiple sclerosis.

Researchers from the University of Calgary in Alberta treated 10 patients with relapsing-remitting multiple sclerosis with the drug minocycline. Patients had a magnetic resonance imaging (MRI) performed before the study and then four weeks later.

Luanne Metz, M.D., lead author of the study, reports that the drug seems to significantly reduce the activity of lesions in the brain. They believe the drug, an antibiotic, works on the immune system of this group of individuals who are known to have immune system malfunctions that trigger the attacks in the nervous system. Dr. Metz says these findings could lead doctors to a new and safe treatment option for patients with MS.

Dr. Metz and colleagues are currently involved in another study looking at the benefits of minocycline when combined with Copaxone, also known as glatiramer acetate, a drug approved to treat MS.

Multiple sclerosis is a chronic, disabling disease that affects one in every 10,000 people. Symptoms vary, but include vision problems, numbness in limbs, balance and coordination problems, and loss of muscular control. Although the disease does not typically lead to death, it can destroy quality of life. There is no cure for multiple sclerosis.

SOURCE: Annals of Neurology, 2004;55:756

Minocycline and Copaxone – a useful combination therapy?

31.01.05

Currently, the main disease modifying drugs used to treat relapsing forms of MS are beta interferon and Copaxone. These drugs have been shown to reduce the relapse rate, on average, by around a third. However, some people do not respond well to these drugs and consequently more effective therapies are needed. Minocycline is a type of antibiotic, commonly used to treat acne, which has been shown to reduce MS symptoms in experimental models of the disease. This study investigated the effects of Copaxone, in combination with minocycline on a model of MS.

Mice with an MS-like disease were treated with a combination of Copaxone and minocycline. Low doses were used in order to assess affects on disease severity, rather than completely prevent the MS-like disease. Symptoms were assessed at regular intervals. Samples of brain and spinal cord tissue were then analysed to assess inflammation, damage to myelin (the protective sheath surrounding nerve fibres) and nerve fibre loss – all processes which can occur in MS. Results were compared to healthy mice and those treated with either minocycline or Copaxone, rather than a combination therapy.

Results showed that the combination of Copaxone and minocycline significantly reduced the severity of the MS-like disease. A greater effect was observed with the combination therapy compared to either minocycline or Copaxone administered alone. Slightly lower levels of inflammation, myelin damage and nerve fibre loss were found in those mice treated with the combination of drugs.

Minocycline and Copaxone are thought to exert their effects through different mechanisms, suggesting that combination use may be more effective than when given alone. However, the mechanism for this has not been fully clarified. Few side effects have been reported with human use of minocycline for acne, and it has the advantage of being administered as a tablet, rather than by injection. The need for more effective, disease modifying therapies is increasingly recognised and clinical trials looking at combinations of drug treatments are already underway. Further research is necessary and the authors note that a trial of minocycline in combination with Copaxone, in people with MS, is ongoing in Canada.

This report was published in the Journal of Neuroimmunology, 2004. Vol. 158, pages 213-221.