Myelin destruction due to inflammatory damage of oligodendrocytes (OLs) in conjunction with axonal degeneration is one of the major histopathological hallmarks of multiple sclerosis (MS), a common autoimmune disorder affecting the central nervous system (CNS). Therapies over the last 20 years mainly focus on the immune system and, more specifically, on the modulation of immune cell behavior. It seems to be effective in MS with relapse, while it is of little benefit to progressive MS in which neurodegeneration following demyelination outweighs inflammation. Otherwise, remyelination, as a result of oligodendrocyte production from oligodendrocyte precursor cells (OPCs), is considered to be a potential target for the treatment of progressive MS. In this review, positive effects of remyelination on MS will be discussed in view of the critical role played by thyroid hormone (TH), focusing on the following points: (1) promising treatment of TH on MS that potentially targets to remyelination; (2) the active role of TH that is able to promote remyelination; (3) the regulative role of TH that works on endogenous stem and precursor cells; (4) the effect of TH on gene transcription; and (5) a working hypothesis which is developed that TH can alleviate MS by promoting remyelination, and the mechanism of which is its regulative role in gene transcription of OPCs.

Lactate is an energy substrate in adult brain especially when glucose is withdrawn or only lactate is present as main energy source. Besides, the most abundant lactate transporter in brain-monocarboxylate transporter 1 (MCT1)-was recognized recently. Despite this, MCT1 expressions in central nervous system (CNS) have not been clearly understood. Medial prefrontal cortex (mPFC), taking part in many higher executive functions in brain, is chosen here for observing MCT1 expressions in mice in 12 months. As results showed, MCT1 is gradually increased from an initial level at the 1st week to a high level at the 6th week and then gradually decreased to a low level at the 12th month. Besides, neuronal amounts change in a similar trend as MCT1 that neurons at the 6th week are more than that of at the 1st week and the 12th month. Also, MCT1 expressions are highly correlated with neuronal amounts, while MCT1 does not localize within neurons, instead localize around axons. On the other hand, MCT1 does localize to oligodendrocytes (OLs) without localizing to other glial cells (astrocytes and microglias). Importantly, the amounts of OLs change in a similar trend as MCT1, while the amounts of other glial cells do not change obviously in the mPFC in vivo in 12 months. These results demonstrate that the changeable expressions of MCT1 in the mPFC in vivo in 12 months may be mainly contributed by OLs and associate with the neuronal amounts. Above all, it infers that in vivo, MCT1 which is changeably expressed in OLs may further affect neuronal amounts in the mPFC in 12 months.