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Old 03-23-2008, 08:50 AM #14
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mrsD mrsD is offline
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Join Date: Aug 2006
Location: Great Lakes
Posts: 33,508
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Default There is a trial

going on using Vit C in CMT patients... I'd ask your neuro about it.

http://lpi.oregonstate.edu/ss06/charcotmarietooth.html

Quote:
Neuromuscul Disord. 2007 Mar;17(3):248-53. Epub 2007 Feb 15.Click here to read Links
Ascorbic acid inhibits PMP22 expression by reducing cAMP levels.
Kaya F, Belin S, Bourgeois P, Micaleff J, Blin O, Fontés M.

INSERM UMR491, Centre de Thérapie Génique, Génomique et de Biothérapies (CTGGB), IPHM-IFR125, Faculté de Médecine de la Timone, 27 bd Jean Moulin, 13385 Marseille cedex 5, France.

Charcot-Marie-Tooth [CMT] syndrome is the most common hereditary peripheral neuropathy. CMT1A, which accounts for 50% of all CMT cases, usually results from triploidy of the PMP22 gene. Preclinical trials using an animal model show that disabled mice force-fed with high doses of ascorbic acid partially recover muscular strength after a few months of treatment, and suggest that high doses of ascorbic acid repress PMP22 expression. In this study, we demonstrated that ascorbic acid represses PMP22 gene expression by acting on intracellular cAMP levels and adenylate cyclase activity. This action is dose dependent and specific to ascorbic acid, since repression is not observed after treatment with other antioxidants. The new properties of ascorbic acid are discussed, along with the implications of these findings for CMT disease treatment.

PMID: 17303424 [PubMed - indexed for MEDLINE]
and this older one:
Quote:
Nat Med. 2004 Apr;10(4):396-401. Epub 2004 Mar 21.Click here to read Links
Ascorbic acid treatment corrects the phenotype of a mouse model of Charcot-Marie-Tooth disease.
Passage E, Norreel JC, Noack-Fraissignes P, Sanguedolce V, Pizant J, Thirion X, Robaglia-Schlupp A, Pellissier JF, Fontés M.

Institut National de la Santé et de la Recherche Médicale UMR491, IPHM, Faculté de Médecine de la Timone, 27 Bd. J. Moulin, 13385 Marseille Cedex 5, France.

Charcot-Marie-Tooth disease (CMT) is the most common hereditary peripheral neuropathy, affecting 1 in 2,500 people. The only treatment currently available is rehabilitation or corrective surgery. The most frequent form of the disease, CMT-1A, involves abnormal myelination of the peripheral nerves. Here we used a mouse model of CMT-1A to test the ability of ascorbic acid, a known promoter of myelination, to correct the CMT-1A phenotype. Ascorbic acid treatment resulted in substantial amelioration of the CMT-1A phenotype, and reduced the expression of PMP22 to a level below what is necessary to induce the disease phenotype. As ascorbic acid has already been approved by the FDA for other clinical indications, it offers an immediate therapeutic possibility for patients with the disease.

PMID: 15034573 [PubMed - indexed for MEDLINE]
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