mTOR Linked to Myelin Repair

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MS lesionsThe axons of nerve cells are sheathed by an insulating layer of myelin which is made up of about 80% lipid and 20% protein. Demyelination, leading to impaired or lost conduction of signals along the nerve, is a hallmark of multiple sclerosis (MS). In relapsing-remitting MS myelin can be replaced but, after repeated attacks, the repair system becomes less efficient. Researchers at the University of Medicine and Dentistry of New Jersey have now identified a key pathway which regulates the production of new oligodendrocytes – the myelin-producing cells of the CNS – and the production of myelin. They found that activation of the mammalian target of rapamycin (mTOR) is essential for oligodendrocyte differentiation at the late progenitor to immature oligodendrocyte transition. The effects were found to be mediated via two distinct signalling complexes, mTORC1 and mTORC2. mTORC2 was found to control myelin gene expression at the mRNA level whereas mTORC1 influenced expression of myelin basic protein via an alternative mechanism.

Although it remains to be determined whether stimulation of the mTOR pathway or removal of some inhibitory mechanism would be most appropriate, allowing the pathway to function normally could provide new treatments for MS and other demyelinating diseases.

The study is published in the May 13th online edition of the Journal of Neuroscience.


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