This Is MS Multiple Sclerosis Community: Knowledge & Support

CONCLUSIONS/RELEVANCE: The results of this study demonstrate a significant association between HDL level classification and disability. While it appears as though the anti-inflammatory effect of high HDL may be protective in patients with MS, further studies regarding the relationship between HDL levels, DMTs and MS disease progression are warranted.

CONCLUSIONS/RELEVANCE: Gender differences in the metabolism of Vitamin D suggest a higher protective effect of Vitamin D-based therapeutic strategies in women

CONCLUSIONS/RELEVANCE: The higher the [Glu] the more neuro-axonal compromise in grey matter is expected over time. This effect was not observed in white matter. The quasi-lack of decline of [NAA]NAWM is consistent with brain volume results where minimal white matter volume decline were reported compared to grey matter. These in vivo findings, from the largest longitudinal analysis of metabolites to date, strongly support the link between the excess of glutamate and decline of neuro-axonal integrity in MS.

CONCLUSIONS/RELEVANCE: Quantitative assessment by R2* relaxometry confirms an increased deposition of iron in the basal ganglia of MS patients which is associated with disease duration and brain atrophy. This technique together with long-term follow-up should also serve to clarify whether regional iron deposition contributes to tissue loss in MS or merely reflects an epiphenomenon of pathophysiological processes of the disease.

CONCLUSIONS/RELEVANCE: IFG, IGT and DM are frequently observed in progressive MS. Disturbances of glucose metabolism may contribute to pathogenesis of progressive MS. The two-hour OGTT is more sensitive than other measures of glucose handling in screening these patients

RESULTS: 22,684 relapses (19,775 northern, 2,909 southern) were included. Relapses were significantly more common in spring in the northern hemisphere (P<0.0001) and autumn in the southern hemisphere (P<0.0001). June had the highest number of relapses than any other month in either hemisphere (P<0.0001).

CONCLUSIONS/RELEVANCE: A highly significant temporal variation in onset of relapses is present in both northern and southern hemispheres. However, peak relapse incidence does not occur in the same season in the northern and southern hemispheres

CONCLUSIONS/RELEVANCE: Tovaxin treatment demonstrated a benefit across clinical and magnetic resonance imaging (MRI) endpoints. The immunology and epitope database assessment suggests that those patients exhibiting a greater T-cell reactivity often demonstrated a worsening of at least one MRI endpoint (Gd lesion, Gd volume, new T2 count or progression to black holes) and one clinical endpoint (either relapse or EDSS). The converse also appears true, where T-cell reactivity resulted in an absence of worsening of MRI and clinical endpoints.

CONCLUSIONS/RELEVANCE: This pilot study suggests that GA 20 mg SC administered QD or QOD may be equally effective in RRMS. Larger, multi-center studies are warranted to confirm our findings and identifying the optimal dose of GA in RRMS.

CONCLUSIONS/RELEVANCE: This small population, proof of concept suggests that targeting mast cells could provide a therapeutic option for both PPMS and SPMS patients. Data give ground for a large scale phase 3 trial

CONCLUSIONS/RELEVANCE: These results demonstrate that reduced NAA levels in NAGM are predictive of future axonal loss in the AVP. This is the strongest in-vivo evidence to date of a relationship between NAA and OCT in MS. Furthermore, this study documents that RNFL thickness is correlated with MRI lesion volume and whole brain volume measures. This provides additional evidence regarding the utility of OCT as a clinic-based correlate of brain injury in MS.

CONCLUSIONS/RELEVANCE: The neuroprotective potential of PBMCs is defective in patients with RRMS as they produce lower neurotrophins mRNA and lack of up-regulatory effect via CD3 and CD40. TNF- may partially restore the levels of the neurotrophins mRNA.

CONCLUSIONS/RELEVANCE: These findings support axonal loss as the pathological substrate of progressive disability in both PP and SP MS with a common plaque-centred mechanism. More extensive axonal loss within white matter plaques in PPMS could explain high levels of axonal loss observed in these patients despite low levels of demyelination.

CONCLUSIONS/RELEVANCE: A diet rich in fish protects against demyelination and clinical signs of demyelination induced by cuprizone. There was, however, no effect of giving omega-3 supplementation in the form of cod liver oil.

CONCLUSIONS/RELEVANCE: This small population, proof of concept suggests that targeting mast cells could provide a therapeutic option for both PPMS and SPMS patients. Data give ground for a large scale phase 3 trial

RESULTS: Of the 35 patients enrolled, 27 received masitinib (10 PPMS and 17 SPMS patients) and 8 received placebo (5 PPMS and 3 SPMS patients). At month 3, patients receiving masitinib improved their MSFC z-scores while a worsening occurred in patients receiving placebo (+78% and -64%, respectively, p=0.321). Both PPMS and SPMS patients receiving masitinib improved their mean MSFC z-scores (+108% and +60%, respectively) whereas it worsened in patients receiving placebo (-14% and -113%, respectively). This improvement was sustainable until month 18 for PPMS and SPMS patients receiving masitinib (+134% and +73%, respectively) compared to PPMS and SPMS patients receiving placebo (-11% and -110%, respectively). This sustainable improvement was mainly driven by T25FW and 9-HPT. Over 18 months of treatment, EDSS scores remained stable in the PPMS population in both treatment groups, while in the SPMS population, EDSS scores remained stable in the masitinib group and increased by one point in the placebo group (p=0.055).

AB Science's lead drug candidate, masitinib, is currently under registration with the EMEA and the FDA for canine mast cell tumors, and it is also in Phase III development for canine inflammatory bowel disease. In human medicine, a European Phase II study showed masitinib to be a safe and effective treatment for mastocytosis, In 2009, AB Science will be conducting ten Phase II studies in colon cancer, prostate cancer, lung cancer, breast cancer, GIST, melanoma, interstitial cystitis, asthma, chronic obstructive pulmonary disease, multiple sclerosis, depression, pulmonary arterial hypertension, and muscular dystrophy as well as several early-stage and preclinical programs various oncology, inflammatory, and neurological indications.

Does anyone have information about the drug MASTINIB (what is it, is it commercially available)? I did some googeling but couldnt find anything useful.

Background: Masitinib mesylate (MM; AB1010) is a protein tyrosine kinase inhibitor (tki) which, in vitro, has greater activity and selectivity than imatinib mesylate (IM) against the wild-type c-Kit receptor and the mutated form in the juxtamembrane region. MM also inhibits the PDGF and FGFR3 receptors.

Imatinib is a drug used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN).
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Gleevec, which costs $32,000 per year for a 400 mg/day dose, is often cited as an example of pharmaceutical industry innovation that justifies the high cost of drugs.

According to AB Science, this drug will cure cancer and IBS in dogs, along with every human disease.

If you were younger I'd give you a kiss to say thank you