Research: Neural Stem Cells with limited activity in repair

Epub: Payne et al. Comparative study on the therapeutic potential of neurally differentiated stem cells in a mouse model of multiple sclerosis. PLoS One. 2012;7(4):e35093.

BACKGROUND: Transplantation of neural stem cells (NSCs) is a promising novel approach to the treatment of neuroinflammatory diseases such asmultiple sclerosis (MS). NSCs can be derived from primary central nervous system (CNS) tissue or obtained by neural differentiation of embryonic stem (ES) cells, the latter having the advantage of readily providing an unlimited number of cells for therapeutic purposes. Using a mouse model of MS, we evaluated the therapeutic potential of NSCs derived from ES cells by two different neural differentiation protocols that utilized adherent culture conditions and compared their effect to primary NSCs derived from the subventricular zone (SVZ).

METHODOLOGY/PRINCIPAL FINDINGS: The proliferation and secretion of pro-inflammatory cytokines by antigen-stimulated splenocytes was reduced in the presence of SVZ-NSCs, while ES cell-derived NSCs exerted differential immunosuppressive effects. Surprisingly, intravenously injected NSCs displayed no significant therapeutic impact on clinical and pathological disease outcomes in mice with experimental autoimmune encephalomyelitis (EAE) induced by recombinant myelin oligodendrocyte glycoprotein, independent of the cell source. Studies tracking the biodistribution of transplanted ES cell-derived NSCs revealed that these cells were unable to traffic to the CNS or peripheral lymphoid tissues, consistent with the lack of cell surface homing molecules. Attenuation of peripheral immune responses could only be achieved through multiple high doses of NSCs administered intraperitoneally, which led to some neuroprotective effects within the CNS.

CONCLUSION/SIGNIFICANCE: Systemic transplantation of these NSCs does not have a major influence on the clinical course of rMOG-induced EAE. Improving the efficiency at which NSCs home to inflammatory sites may enhance their therapeutic potential in this model of CNS autoimmunity.



This study contrasts with other previous reports suggesting some immunomodulatory effects, but shows no or minimal immunomodulatory effect and no evidence that they form myelin producing cells, which is what is needed. They fail to home into areas of damage. Another example to support the hype of stem cells. There will be other papers that claim benefit but we need to look hard at what they are actually showing and what is not being shown

There is a long way to go before we know how to control the transplanted cells such that they can be delivered via the blood and home to where they are needed. Then they need to produce repair cells and repair.

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