Thyroid hormones promote differentiation of oligodendrocyte progenitor cells and improve remyelination

Just wondering if this might be of interest to those suffering from demylenination?

Exp Neurol. 2008 Aug;212(2):458-67. doi: 10.1016/j.expneurol.2008.04.039. Epub 2008 May 15.

Thyroid hormones promote differentiation of oligodendrocyte progenitor cells and improve remyelination after cuprizone-induced demyelination.

Franco PG1, Silvestroff L, Soto EF, Pasquini JM.

Author information


In the present work we analyzed the capacity of thyroid hormones (THs) to improve remyelination using a rat model of cuprizone-induced demyelination previously described in our laboratories. Twenty one days old Wistar rats were fed a diet containing 0.6% cuprizone for two weeks to induce demyelination. After cuprizone withdrawal, rats were injected with triiodothyronine (T3). Histological studies carried out in these animals revealed that remyelination in the corpus callosum (CC) of T3-treated rats improved markedly when compared to saline treated animals. The cellular events occurring in the CC and in the subventricular zone (SVZ) during the first week of remyelination were analyzed using specific oligodendroglial cell (OLGc) markers. In the CC of saline treated demyelinated animals, mature OLGcs decreased and oligodendroglial precursor cells (OPCs) increased after one week of spontaneous remyelination. Furthermore, the SVZ of these animals showed an increase in early progenitor cell numbers, dispersion of OPCs and inhibition of Olig and Shh expression compared to non-demyelinated animals. The changes triggered by demyelination were reverted after T3 administration, suggesting that THs could be regulating the emergence of remyelinating oligodendrocytes from the pool of proliferating cells residing in the SVZ. Our results also suggest that THs receptor beta mediates T3 effects on remyelination. These results support a potential role for THs in the remyelination process that could be used to develop new therapeutic approaches for demyelinating diseases.



[PubMed - indexed for MEDLINE]


10 Replies

  • Oh, it just might be me - but wouldn't it be preferable for one of these research groups to actually try giving patients enough b12 to enduce remyelination rather than giving them enough to top up their blood levels.

    It's a handy article H, but honestly, the fact that they won't trial b12 with regard to this issue particularly since it's b12 which affects myelin in the first place, is starting to drive me crazy.

  • Fully agreed re B12. Reason I posted was thinking that if adequate levels of both B12 and T3 are required, which might well be higher that the medical establishment can get their heads round, then it would be folly to treat with only one.

    Have now fallen across some use of poly (dextrogyr-levogyr) lactide acid-triiodothyronine to create a scaffold for nerve regeneration:

    Which triggers even greater suspicion of the importance of T3 in nerve and Schwann cells.


  • I wasn't having a go at you, Helvella, it was a good thing to post - but if they aren't trialing b12 when b12 is a known cause...

    They did the same thing with folate and that went on for decades. Folate deficiency was the root of all evil...oh no, actually folate deficiency is only a problem resulting from b12 deficiency and anyway, neurological damage resulting from folate deficiency is reversible.

    Drives me nuts.

    They have to rule out an obvious cause before looking at other possibilities and influencing factors.

    If we took notice of what everyone said, the lot of us would be swallowing enough tablets to make us rattle.

  • Don't worry Poppet, I have been around Usenet and forums too long to easily feel got at! :-)

    I see so many reports of thyroid people with levels of B12 that are low but (usually) over bottom of range for serum B12, I always think of the the issues as intimately related. But that is my bias! Nevertheless, most get told all is well with their B12.

  • I keep repeating this because I think it's important - the thyroid is a balancing mechanism. If something in the body is sending the metabolism out, then the thyroid will be forced to make constant readjustments.

    We know that they are only giving enough b12 to bring blood levels up but not to sort out the metabolic issues - so to me it seems common sense that the thyroid will still fluctuate.

    I could be completely wrong! But until they sort out the issues with b12 and start giving people the correct doseage, then we will still be left with the situation that so many people appear to have had their b12 levels 'treated' but are still suffering thyroid problems.

    Of course that still doesn't answer the big question - why are so many people developing b12 deficiency in the first place?

  • Same question in thyroid world. Why so many with hypothyroidism?

    I suspect that many in thyroid world suffer B12D due to low stomach acidity, low digestive enzymes, gastric parietal cell antibodies (though it sometimes looks as if these might be transient in some), and poorly functioning gut - on top of any other factors which would apply outwith thyroid world.

    Also - so many have tried very hard to lose weight so may have had compromised intake. And the numerous intolerances and similar which many thyroidally challenged people have.

  • We are in absolute agreement!

    It's not only thyroid and b12 - it's any mineral or vitamin which necessitates stomach acid to be absorbed or any knock on effects that might result from malabsoption.

    But again, the big question - why all the low stomach acid?

    Something, that in Europe, there isn't even a test for!

  • I see it as low thyroid directly causing low stomach acid. It takes a lot of energy to make that stomach acid and insufficient thyroid hormone seems to make it difficult to create enough.

    We also see many who have been prescribed PPIs and H2As and other medicines which suppress stomach acid production. It can be difficult to decide whether someone has too little or too much (as you say, without a formal test). Low thyroid also seems to be behind many cases of hiatus hernia which can result in reflux (thyroid can cause a weakened lower oesophageal sphincter). A doctor seeing reflux has a reflex action - prescribe PP1 or H2A. Which only makes it worse. Many actually do much better by taking apple cider vinegar and/or betaine HCL.

  • But if your supposition is correct then even patients who take ACV would still have thyroid problems.

    I've had a formal test for stomach acid and it was low.

    But my thyroid level corrected when I started the b12 (self medicating not prescribed) and ACV.

    There has to be a direct physiological or biological link between thyroid and stomach acid, yet thyroid is not a controlling mechanism, it's reactionary.

    I would dispute that thyroid is 'behind' cases of hiatus hernia - it's no more relevant than the links between low stomach acid and vit d deficiency or iron. All of them are associated either directly or indirectly with low stomach acid but none are considered a cause of low stomach acid.

    The only way to resolve the issue is actually to test people for low stomach acid and treat them. If all the malabsorption issues improve then that would be considered to be the source of the problem. If thyroid issues resolved also then that would no longer have be necessary to consider it, or any of the other malabsorption problems as being causative.

    I think also you have to consider that it becomes a cyclical argument. Many people who are prescribed PPIs take other remedies for long periods before they are prescribed PPIs.

    Some of us have rarely taken any OTC or prescribed medication for indigestion.

    I'm not arguing that it doesn't make the problem worse because it's clearly a major contributory factor to increasing the prevelance of low stomach acid.

    Like I said earlier, if we listened to everyone about what we should be taking - we'd rattle.

    I'd be on thyroid meds, cholesterol, folic acid, calcium, vit d3, iron... oh, and correspondingly minute amount of b12.

    What we seem to forget is that under normal circumstances these are micro elements. The human body needs only small amounts to function effectively. If, as is now suggested, at least 1 in 3 people are suffering from a b12 deficiency and, as you suggest that in turn is caused by low stomach acid resulting from a thyroid problem, then I would suggest the human race is heading for a collapse.

    I think the problem is much closer to home and much less complicated.

  • That's useful to know

    Re T3

    Also remyelination one must not forget thiamine ( oral doesn't work well ) and Nicatonic acid which Dr . mount in UK and Dr Kleener Md ( America ) used for MS with good results .

    I will dig the papers out and post during the week

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