Multiple sclerosis is characterized by multiple lesions in brain and spinal cord which are the result of demyelination, inflammation, gliosis and axonal damage. The underlying cause for the permanent neurological deficits in Multiple Sclerosis patients is axonal loss. Demyelinated axons are prone to damage due to the lack of trophic support by myelin sheaths and oligodendrocytes, as well as the increased vulnerability to immune mediated attacks. Remyelination occurs, but especially in chronic lesions is frequently limited to a small rim at the lesion border. Current treatment strategies are based on anti-inflammatory or immunomodulatory drugs and have the potential to reduce the numbers of newly evolving lesions, although as yet no treatment strategy exists to influence or prevent the progressive disease phase. Therefore, the development of neuroprotective treatment options, such as the promotion of endogenous remyelination is an attractive strategy. This review discusses mechanisms leading to remyelination and the reasons for insufficient endogenous repair in chronic Multiple Sclerosis.
Hagemeier K, Brück W, Kuhlmann T: Multiple Sclerosis – remyelination failure as a cause of disease progression. Histol. Histopathol. 27(3): 277-287 (2012).
http://www.ncbi.nlm.nih.gov/pubmed/22237705
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Given that remyelination is an important factor in Multiple Sclerosis drug development, the following report presents useful data on thyroxine’s effects in this regard. Cuprizone-induced cortical demyelination in rodents produces lesions similar to those found in Multiple Sclerosis patients. Treatments such as intranasal Thyroid hormone were found to accelerate the remyelination rate compared to non-drug treated controls. Extension of these studies to Multiple Sclerosis patients may provide a strategy to promote the remyelination process in the cortex and to prevent irreversible neuronal damage in patients suffering from Multiple Sclerosis.
Silvestroff L, Bartucci S, Pasquini J, Franco P: Cuprizone-induced demyelination in the rat cerebral cortex and thyroid hormone effects on cortical remyelination. Exp. Neurol. 235(1): 357-367 (2012).
