Selective Diabetes Typ I treatment

Frank

The method modulates the TNF activity to stop the ongoing damage.
When dissease activity is halted the animals were able to regrow functioning islet cells.
Animal studies were successful, first clinical trials are underway:

http://www.sciencedaily.com/releases/2008/08/080825175001.htm

--Frank
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Current regime: Tysabri restarted 05/2008 after LDN, ABX Wheldon Regime for 1 year, interested in T-Cell vaccination, helminth immunomodulation

Lyon · Posted: Tue Aug 26, 2008 3:23 pm Post subject:

Thanks Frank, although I wish they went into more detail about how it works, that one is very interesting and it would be nice to hear more about it in the future.

Bob
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Wife diagnosed with MS in Feb. 2006 and is a participant in the Tovaxin IIb clinical trial.

gibbledygook · Posted: Wed Aug 27, 2008 1:19 am Post subject:

Here's a chinese herb that upregulates beta interferon and tumour necrosis factor alpha in certain breast cancer cell lines:

NHE · Volunteer Moderator Joined: Nov 21, 2004 Posts: 760

The whole issue with TNF is particularly interesting as early studies with TNF blocking antibodies were found to increase lesion activity. It will be interesting to see what this new compound will do for MS patients.

Increased MRI activity and immune activation in two multiple sclerosis patients treated with the monoclonal anti-tumor necrosis factor antibody cA2. Neurology. 1996 Dec;47(6):1531-4.

There is evidence that treatment with an antibody to tumor necrosis factor alpha (TNF alpha) improves an animal model of multiple sclerosis (MS) and is beneficial in two systemic inflammatory disease in humans, but there are no reports about anti-TNF treatment of MS. Therefore, we treated two rapidly progressive MS patients with intravenous infusions of a humanized mouse monoclonal anti-TNF antibody (cA2) in an open-label phase I safety trial and monitored their clinical status, gadolinium-enhanced brain magnetic resonance imaging (MRI), and peripheral blood and cerebrospinal fluid (CSF) immunologic status. We did not notice any clinically significant neurologic changes in either patient. The number of gadolinium-enhancing lesions increased transiently after each treatment in both patients. CSF leukocyte counts and IgG index increased after each treatment. The transient increase in the number of gadolinium-enhancing lesions that followed each infusion of cA2 together with the increase in cells and immunoglobulin in the CSF of each patient suggest that the treatment caused immune activation and an increase in disease activity. These results suggest that further use of cA2 in MS is not warranted and that studies of other agents that antagonize TNF alpha should be carried out with frequent monitoring of gadolinium-enhanced MRIs.

Another early study in secondary progressive MS patients found no benefit to blocking TNF.

Randomized study of antibodies to IFN-gamma and TNF-alpha in secondary progressive multiple sclerosis.
Mult Scler. 2001 Oct;7(5):277-84.

Studies of cytokines in multiple sclerosis (MS) have shown that immune mechanisms connected with disturbance of the synthesis of cytokines probably play critical roles in the initiation and prolongation of MS. In a double-blind, placebo-controlled trial, 45 patients with active secondary progressive MS were randomized to three groups of 15 patients, each receiving a short course of antibodies to IFN-gamma, to tumor necrosis factor (TNF)-alpha, or a placebo. After 12 months with analysis of disability (Expanded Disability Status Scale scores), accompanied by interval determinations of lymphocyte subpopulations, cytokine production levels, MRI, and evoked potentials, it was found that only patients who received antibodies to IFN-gamma showed statistically significant improvement compared to the placebo group--a significant increase in the number of patients without confirmed disability progression. This was supported by MRI data (a decrease in the number of active lesions) and systemic changes in cytokine status (a decrease in IL-1beta, TNF-alpha, and IFN-gamma concentrations in supernatants of actvated blood cells of these MS patients and an increase in TGF-beta production). Neutralization of IFN-gamma could be a new approach to treating secondary progressive MS. Long-term administration of humanized monoclonal antibodies to IFN-gamma and simultaneous use of antibodies to IFN-gamma together with IFN-beta products are planned.

NHE

gibbledygook · Posted: Tue Sep 02, 2008 8:41 am Post subject:

Here's the pubmed citation: