Neural Precursor Cells Induce Repair of Myelin Loss in Mice

Myelin is the sheathing of nerves, and loss of myelin contributes to a number of debilitating diseases. This loss is also shown to occur to a lesser degree in aging, so just as for many types of disease it is worth keeping an eye on the progression of treatments such as the one discussed here. This paper is open access, but the full version is in PDF format only at the moment.

Using a viral model of the demyelinating disease multiple sclerosis (MS), we show that intraspinal transplantation of human embryonic stem cell-derived neural precursor cells (hNPCs) results in sustained clinical recovery, although hNPCs were not detectable beyond day 8 posttransplantation. Improved motor skills were associated with a reduction in neuroinflammation, decreased demyelination, and enhanced remyelination.

In summary, we demonstrate that transplantation of hNPCs into a mouse model of viral-induced demyelination results in prolonged clinical recovery up to at least 6 months in spite of the disappearance of transplanted hNPCs after only a week. Our findings extend the existing evidence that long-term engraftment is not important for sustained clinical and histologic recovery. Our evidence points to secreted factors produced by the hNPCs in the local environment as the regulators of T cell fate and remyelination activity by endogenous OPCs. Because they are produced by the hNPCs used in our study and have known effects on T cell development, members of the TGF-b family are strong candidates as triggers initiating clinical recovery.

As an aside, note that this is one of numerous studies in which the benefits derived from cell therapies are shown to have little to do with ongoing activities of the transplanted cells themselves. The cells change the environment and behavior of native cells even when they are only present for a comparatively short time.



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