Monday, 19 March 2012

Research;Experimental Remyelination by Thyroid Hormones

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. 2012 Mar [Epub ahead of print]
Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the Central Nervous System which is characterized by multifocal demyelinated lesions dispersed throughout the brain. Although white matter lesions have been the most extensively studied, cortical demyelinaton lesions are also detected in MS brains. Cuprizone (CPZ)-induced demyelination in rodents has been widely used as a model for MS. Most of these studies focus on oligodendrocyte-rich structures, such as the corpus callosum (CC) and the cerebellar peduncles. However, it has been recently described that CPZ administration in mice also produces cortical demyelination, resembling some of the lesions found in MS patients. In this work, we used CPZ-demyelinating model in Wistar rats, to study demyelination in cortical forebrain areas. At the ultrastructural level, demyelination in the cortex was observed before detectable myelin loss in the subcortical white matter. During the course of CPZ intoxication Myelin Basic Protein immunodetection was decreased in cortical layers I-III due to a reduction in the number of cortical oligodendrocytes (OL). Oligodendroglial loss in CPZ-intoxicated rats correlated with an increase in the number of Glial Fibrillary Acidic Protein positive astrocytes and a shift in the location of Carbonic Anhydrase II from OL to astrocytes. After removal of CPZ from the diet, we evaluate intranasal Thyroid hormone (TH) effects on the progression of cortical lesions. As previously reported in the CC, TH treatment also accelerates remyelination rate in the cortex compared to rats undergoing spontaneous remyelination. Our results suggest that manipulation of TH levels could be considered

For years and years cuprizone, which is an oligodendrocyte killing chemical (toxin) , was only thought to affect the cerebellar peduncle, then it affected the corpus callosum, which is the bridge between the left and right sides of the brain, and as MS has moved from being a white matter disease to be a grey and white matter disease, it is interesting that cuprizone also demyelinates grey matter. This study reports that snorting thyroid hormone promotes recovery of myelin. There have been a number of studies looking at the effect of thyroid hormone on myelin forming cells in experimental myelin repair. However, the influence of tyroid hormone on remyelination in humans is limited. This is a testable effect as thyroid disease, requiring thyroid hormone supplementation is common. Thyroid disease occurs in 22% of people, about 12-18 months after, taking alemtuzumab, this is Graves disease and is hyperactive and following treatment to kill off or remove the thyroid people recive supplements of thyroid hormone. So does anyone taking thyroid hormone feel like it is making their MS better?


  1. I may be in a minority of one, but in my case, I have to downregulate my thyroid med or my MS flares. This has now been tested over a decade with all the different thyroid medications and with different dosages, and the evidence is clear. Strange, but true. But then MS itself is a strange disease.

  2. Mouse,

    The issue with Alemtuzumab is that it gives some patients Graves' disease - over-active thyroid. The thyroid has to be calmed down and potentially killed off (radio-active iodine). Once the radio-active iodine has done its job, the thyroid eventually becomes under-active and thyroid replacement is required.

  3. Oops you are right......My Brain Fart


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