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Postby Nickmare » Mon May 17, 2010 1:51 pm

Hey all,

My fiance has ADEM or MS (unsure as this is her first attack of this nature) and become completely paralyzed as a result. She's been in the hospital approximately 2 months and she has started to recover (can swallow pureed food, move right hand a bit, move feet, and move her neck).

The doctors have no plans for her recovery other then speech therapy and physiotherapy. I'm just wondering if anyone has any ideas on what could help with remyelination during her recovery phase? Is there anything more we can do to help her chances at a better recovery?

Are there any drugs which could help right now or are they all under study currently?

Thanks all
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Postby dignan » Mon May 17, 2010 10:02 pm

Nickmare, I'm really sorry to hear about your fiance's situation. There aren't any formally approved treatments for remyelination. A while ago the remyelination issue came up and I found a couple of possibilities. Also in the same thread ( ... ion-0.html), Shayk came up with a couple of other options:

1. Cannabinoids

Therapeutic Action of Cannabinoids in a Murine Model of Multiple Sclerosis

Angel Arevalo-Martın, Jose Miguel Vela, Eduardo Molina-Holgado, Jose Borrell, and Carmen Guaza
Neuroimmunology Group, Neural Plasticity Department, Cajal Institute, Consejo Superior de Investigaciones Cientıficas, 28002 Madrid, Spain, and Unit of Histology, School of Medicine, Department of Cell Biology, Physiology, and Immunology, Universidad Autonoma de Barcelona, 08193 Bellaterra, Barcelona, Spain

Theiler’s virus infection of the CNS induces an immune-mediated demyelinating disease in susceptible mouse strains and serves as a relevant infection model for human multiple sclerosis (MS). Cannabinoids may act as immunosuppressive compounds that have shown therapeutic potential in chronic inflammatory disorders. Using the Theiler’s murine encephalomyelitis virus model, we report here that treatment with the synthetic cannabinoids WIN 55,212–2, ACEA, and JWH-015 during established disease significantly improved the neurological deficits in a long-lasting way. At a histological level, cannabinoids reduced microglial activation, abrogated major histocompatibility complex class II antigen expression, and decreased the number of CD4 infiltrating T-cells in the spinal cord. Both recovery of motor function and diminution of inflammation paralleled extensive remyelination. Overall, the data presented may have potential therapeutic implications in demyelinating pathologies such as MS; in particular, the possible involvement of cannabinoid receptor CB2 would enable nonpsychoactive therapy suitable for long-term use.

To read the entire article:

2. Polyunsaturated fatty acids

Polyunsaturated fatty acid supplementation stimulates differentiation of oligodendroglia cells.

Dev Neurosci. 2006;28(3):196-208.
van Meeteren ME, Baron W, Beermann C, Dijkstra CD, van Tol EA.
Biomedical Research Department, Numico Research B.V., Wageningen, The Netherlands.

Dietary polyunsaturated fatty acids (PUFAs) have been postulated as alternative supportive treatment for multiple sclerosis, since they may promote myelin repair. We set out to study the effect of supplementation with n-3 and n-6 PUFAs on OLN-93 oligodendroglia and rat primary oligodendrocyte differentiation in vitro.

It appeared that OLN-93 cells actively incorporate and metabolise the supplemented PUFAs in their cell membrane. The effect of PUFAs on OLN-93 differentiation was further assessed by morphological and Western blot evaluation of markers of oligodendroglia differentiation: 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP), zonula occludens-1 (ZO-1) and myelin-associated glycoprotein (MAG). Supplementation of the OLN-93 cells with n-3 and n-6 PUFAs increased the degree of differentiation determined by morphological analysis. Moreover, CNP protein expression was significantly increased by gamma-linolenic acid (GLA, 18:3n-6) supplementation.

In accordance with the OLN-93 results, studies with rat primary oligodendrocytes, a more advanced model of cell differentiation, showed GLA supplementation to promote oligodendrocyte differentiation. Following GLA supplementation, increased numbers of proteolipid protein (PLP)-positive oligodendrocytes and increased myelin sheet formation was observed during differentiation of primary oligodendrocytes. Moreover, increased CNP, and enhanced PLP and myelin basic protein expression were found after GLA administration. These studies provide support for the dietary supplementation of specific PUFAs to support oligodendrocyte differentiation and function.

From Shayk:

3. thyroid hormone

thyroid hormone enhances and accelerates remyelination in an experimental model of chronic demyelination

Thyroid hormone, when administered during the acute phase of the disease, increases expression of platelet-derived growth factor alpha receptor, restores normal levels of myelin basic protein mRNA and protein, and allows an early and morphologically competent reassembly of myelin sheaths. Moreover, thyroid hormone exerts a neuroprotective effect with respect to axonal pathology.


4. progesterone

In addition to its traditional role in reproduction, progesterone (PROG) has demonstrated neuroprotective and promyelinating effects in lesions of the peripheral and central nervous systems, including the spinal cord.

Earlier research :
PROG also promotes myelination in the brain, as shown in vitro in explant cultures of cerebellar slices and in vivo in the cerebellar peduncle of aged rats after toxin-induced demyelination.

Local synthesis of PROG in the brain and the neuroprotective and promyelinating effects of this neurosteroid offer interesting therapeutic possibilities for the prevention and treatment of neurodegenerative diseases, for accelerating regenerative processes and for preserving cognitive functions during aging.
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Re: Remyelination?

Postby NHE » Tue May 18, 2010 1:35 am

Biogen recently started a phase I trial of an antibody which blocks the function of lingo-1 which has been found to inhibit remyelination. The hoped for effect is that if you block the inhibitor, then the remyelination process should go forward. Phase I studies are still early in a drug's development cycle though it does give some hope as the number of candidates that actually make it to phase I is low. The anti-lingo antibody currently goes by the name BIIB033. Dignan put together a good overview of the history of its development. It's an interesting post to read through.

Here's a link to the study outline on ... gen&rank=1

The study is recruiting healthy volunteer subjects to examine the pharmacokinetics and tolerability of the drug.

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Postby Nickmare » Tue May 18, 2010 2:05 pm

Thanks Dignan and NHE for the great info.

I'll add to the information on remyelination with a study I found from Japan, "Administration of Chinpi, a Component of the Herbal Medicine Ninjin-Youei-To, Reverses Age-induced Demyelination".
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Postby dignan » Tue May 18, 2010 7:23 pm

Here are a couple of other things that could (maybe) help: vitamin B12 and DHEA.


J Immunol. 2001 Dec 15;167(12):7094-101. Links
Administration of dehydroepiandrosterone suppresses experimental allergic encephalomyelitis in SJL/J mice.Du C, Khalil MW, Sriram S.
Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212, USA.

Experimental allergic encephalomyelitis (EAE) is a Th1-mediated inflammatory demyelinating disease in the CNS, an animal model of multiple sclerosis. We have examined the effect of dehydroepiandrosterone (DHEA) on the development of EAE in mice. The addition of DHEA to cultures of myelin basic protein-primed splenocytes resulted in a significant decrease in T cell proliferation and secretion of (pro)inflammatory cytokines (IFN-gamma, IL-12 p40, and TNF-alpha) and NO in response to myelin basic protein. These effects were associated with a decrease in activation and translocation of NF-kappaB. In vivo administration of DHEA significantly reduced the severity and incidence of acute EAE, along with a decrease in demyelination/inflammation and expressions of (pro)inflammatory cytokines in the CNS. These studies suggest that DHEA has potent anti-inflammatory properties, which at least are in part mediated by its inhibition of NF-kappaB activation.

This study is in rats, but still...

Dehydroepiandrosterone as an enhancer of functional recovery following crush injury to rat sciatic nerve.

Microsurgery. 2002;22(6):234-41.
Gudemez E, Ozer K, Cunningham B, Siemionow K, Browne E, Siemionow M.
Department of Plastic Surgery, A60, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

This study was designed to investigate the effect of dehydroepiandrosterone (DHEA) on the recovery of the rat sciatic nerve following crush injury. A standard hemostat system was used to create the injury, with a length of 1.5 mm in three groups of 18 animals each. In group I, the crush injury was applied without any treatment. In groups II and III, vehicle (ethylene glycol) and DHEA solutions were injected subepineurally 30 min following the crush injury. Sciatic function index (SFI), toe contracture measurement, gastrocinemius muscle weight, total number of myelinated fibers, fiber diameters, myelin thickness, and axon/fiber cross-sectional ratio were measured at 3, 6, and 12 weeks. The SFI values in the DHEA group showed a faster return to normal values confirmed at 3 and 6 weeks (P < 0.05). The number of myelinated fibers and fiber diameters at 6 and 12 weeks were significantly higher in the DHEA group (P < 0.05). In this study, the subepineural injection of DHEA following crush injury was found to enhance functional recovery of the rat sciatic nerve.
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