For the past 40 years or so, the repair of myelin in laboratory animals has been proven to occur naturally in a short time. A recent article claims that the use of viagra (sildenafil) reduces the clinical signs of EAE [in mice] by preventing axonal loss and promoting remyelination …” span class=”style3″> AHA! Drug companies have been looking for an excuse to market Viagra to women and it is believed that more women than men have multiple sclerosis, This faulty article might fool some people into thinking that Viagra would help repair of myelin in humans! So what’s up?

Here’s the article … Sildenafil ameliorates clinical symptoms and neuropathology in a mouse model of multiple sclerosis. Pifarre P, Prado J, Baltrons MA, Giralt M, Gabarro P, Feinstein DL, Hidalgo J, Garcia A.
Acta Neuropathol. 2011 Apr;121(4):499-508. doi: 10.1007/s00401-010-0795-6. Epub 2011 Jan 15.

Abstract
Cyclic GMP (cGMP)-mediated pathways regulate inflammatory responses in immune and CNS cells. Recently, cGMP phosphodiesterase inhibitors such as sildenafil(viagra), commonly used to treat sexual dysfunction in humans including multiple sclerosis (MS) patients, have been reported to be neuroprotective in animal models of stroke, Alzheimer’s disease, and focal brain lesion. In this work, we have examined if sildenafil ameliorates myelin oligodendrocyte glycoprotein peptide (MOG35?55)-induced experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. We show for the first time that treatment with sildenafil after disease onset markedly reduces the clinical signs of EAE by preventing axonal loss and promoting remyelination. … results highlight novel actions of sildenafil that may contribute to its beneficial effects in EAE and suggest that treatment with this widely used and well-tolerated drug may be a useful therapeutic intervention to ameliorate MS neuropathology.

NOTE: While lab animals recover, we humans continue to be told that we can expect progressive decline with little hope for recovery, and that we must wait for a chemical miracle …

NOTE:

Raine CS and Bornstein MB, EAE: A Light and Electron Microscopy Study of Remyelination and Sclerosis in Vitro. J Neuropath Exp Neurol 29:552, 1970. total demyelination in living mice embryo tissue cultures … Tissue fragments began to remyelinate after 8 -10 days and process was well advanced by 18 days. By three weeks, almost total remyelination.

Hirano A, Levine S and Zimmerman HM, Remyelination in the Central Nervous System after Cyanide Intoxication. J Neuropath Exp Neurol 27:234-245, 1968. By one week after demyelination [in adult rats] we observed remyelination … recently several fine structural studies have established this phenomenon beyond reasonable doubt. p235

Gledhill R, Harrison BM, MacDonald WI, Demyelination and Remyelination After Acute Spinal Cord Compression. Exp Neurol 38:472-487, 1973. Remyelination in cats commenced 7-21 days after demyelination and majority of demyelinated fibres showed evidence of remyelination by 1month.

Patten Bradley M, Foundations of Embryology. McGraw-Hill Book Company, Inc. New York London Toronto 1958. – Cerebrospinal Conduction Paths. p351 Phylogenetically these [cerebrospinal] conduction paths in the peripheral part of the cord increase in conspicuousness concomitantly with the increasing extent to which the brain assumes a co-ordinating control over the basic reflexes which constitute the primary function of the cord. Paraphrase … the ‘white matter’ or myelin, in the motor part of the cord, develops as the brain assumes control over basic reflexes.
[EM COMMENT: SO since movement promotes myelination, it seems reasonable to me, that movement must also promote re – myelination.]

Harrison BM, McDonald WI and Ochoa J, Remyelination in Central Diphtheria Toxin Lesion. J Neurol Sci 17:293-302, 1972. … even the limited amount of remyelination observed may be sufficient to restore transmission. Although conduction would still be slow in the thinly myelinated fibres, the return of the ability to conduct at all is clearly a necessary first step in the recovery of function in damaged pathways. p301.

 

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