AAN Abstracts for April Meeting

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Shayk
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AAN Abstracts for April Meeting

Post by Shayk »

Hi all

The American Academy of Neurology (AAN) abstracts for the April meeting are up and not embargoed. :) The general web site is here. Some that quickly caught my eye (and there are lots of them) that might be of interest.

[P02.144] Examining the Association between High-Density Lipoprotein Levels and Disability in Patients with Multiple Sclerosis
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.

S39.004] Gender Differences in Immunomodulatory Effects of 1,25 Dihydroxyvitamin D3 in Multiple Sclerosis
CONCLUSIONS/RELEVANCE: Gender differences in the metabolism of Vitamin D suggest a higher protective effect of Vitamin D-based therapeutic strategies in women

S31.004] Brain Atrophy Predicts Disability Progression in Multiple Sclerosis

[S31.002] In Vivo Evidence of Glutamate Toxicity in MS: A Longitudinal Spectroscopy Study
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.

[S51.002] Quantitative Assessment of Brain Iron by R2* Relaxometry in Patients with Clinically Isolated Syndrome or Relapsing Remitting Multiple Sclerosis
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.

P08.038] High Frequency of Impaired Glucose Tolerance and Diabetes in Patients with Progressive Multiple Sclerosis
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

[P08.027] Temporal Variation of Onset of Relapses in Multiple Sclerosis: Results from the Northern and Southern Hemispheres in the MSBase Registry
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

[P06.132] TERMS Trial T-Cell Vaccination Secondary Analysis of Clinical and Immunologic Outcomes in Relapsing Remitting Multiple Sclerosis Patients
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.

[P06.141] Randomized, Prospective, Rater-Blinded, Four Year Pilot Study To Compare the Effect of Daily Versus Every Other Day Glatiramer Acetate 20 mg Subcutaneous Injections in RRMS
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.

[P06.130] Oral Masitinib in Patients with Primary Progressive or Secondary Progressive Multiple Sclerosis
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

[P05.156] Correlation between N-acteylaspartate (NAA) Levels and RNFL Thickness Measures in a Large Multiple Sclerosis (MS) Cohort
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.

[P09.110] Low Production and Defective Regulation of Neurotrophins mRNA in Immune Cells of Patients with RR-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.

[S17.004] Equal Loss of Corticospinal Axons Despite Less Demyelination in Primary Versus Secondary Progressive Multiple Sclerosis
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.

[S47.004] Fish Diet Prevents Demyelination, Clinical Symptoms and MRI Activity in the Cuprizone Model
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.
Lots to check out...just what caught my eye during lunch. Too friggin' cold to go outside. :lol:

Sharon
Frank
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Re: AAN Abstracts for April Meeting

Post by Frank »

Thanks for the compilation, Sharon :)!

This here I found specially interesting:

[P06.130] Oral Masitinib in Patients with Primary Progressive or Secondary Progressive Multiple Sclerosis
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 from the Abstract:
--------------------------------
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).
Does anyone have information about the drug MASTINIB (what is it, is it commercially available)? I did some googeling but couldnt find anything useful.

--Frank
Treatment: Gilenya since 01/2011, CCSVI both IJV ballooned 09/2010, Tysabri stopped after 24 Infusions and positive JCV antibody test, after LDN, ABX Wheldon Regime for 1 year.
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Post by dignan »

Sharon, thanks for posting these. It's always interesting looking through the abstracts. Frank, I did the same thing and didn't come up with much on masitinib either. There is this:
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.
http://www.ambosmedios.com/ebooknews/in ... digest.pdf (page 47)

Another mention of it said it is also known as "AB1010".

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

Sharon,

If you were younger I'd give you a kiss to say thank you. But, my New Year's resolution was to cut down on MS websites and I get sucked in to all the abstract stuff.

Given my interest in EBV ( and Prof Giovannoni who is one of my neuros), the following is of interest:

http://www.abstracts2view.com/aan2009se ... 9L_P01.117

It's nice and Spring like in London this week - sorry it's cold in the US.

Ian
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CureOrBust
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Re: AAN Abstracts for April Meeting

Post by CureOrBust »

Frank wrote:Does anyone have information about the drug MASTINIB (what is it, is it commercially available)? I did some googeling but couldnt find anything useful.
I also did a quick look, and found this small piece / link, don't know if it really helps to answer your question, since it is not the exact same medication.

<shortened url>
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.
http://en.wikipedia.org/wiki/Glivec
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).
....
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.
dignan wrote:According to AB Science, this drug will cure cancer and IBS in dogs, along with every human disease.
including obscene wealth.
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dignan
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Post by dignan »

I was wondering with it being used in dogs if it would be easy to get it "off-label" through a vet...I know it's not approved yet though.
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Shayk
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Post by Shayk »

Ian
If you were younger I'd give you a kiss to say thank you
LOL. All I can do is sort of echo Tina Turner, "What's age got to do with it?"

Hope you're well....miss your humor....and your posts.

Sharon
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Post by Arcee »

Sharon -

Just read these posts and wanted to thank you as well. I was thrilled to see the data about every other day Copaxone as that is what I do. (Too many injection site problems otherwise, and I was suspicious about the daily need.) So I will think about the post during the annoying injections, and maybe they won't be as annoying :)

Thanks,
Arcee
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