Dale Corbett and Dr. Sam Weiss from the Canadian Stroke Network have research

I think it depends on what you mean by 'work'... exist and migrate to the damaged area? integrate into the existing system and become potentially functional (i.e. mature into a specific neural cell type)? or actually exert a measurable functional benefit, and if so, as measured by what? Crazy complicated brains.

Unfortunately, we cannot answer this question, yet. With regard to what Jessy said, these NPCs do actually do the job in terms of proliferation and migration. However, differentiation rates of these cells are low. This and the fact that survival rates are low as well makes integration or genuine cell replacement extremely unlikely - at least for the moment. These cells might be interesting when regarded as "mini-pumps" secreting soluble factors that might induce post-ischemic neuroprotection...

In my opinion one of the main tasks is to influence the injured environment to make it more permissive to migration/differentiation of stem cells. Our work showed that for exemple increasing local oxygen tension helps integration of implanted stem cells in mice stroke model. To cite an old Michelin ad: Power is nothing without control. Although the potential to integrate is given, it does not mean cell-replacement usually

http://www.ncbi.nlm.nih.gov/pubmed/20969864

Even if the cells differentiate, there are still the developmental stages that they would not be able to go through such as fetal development that causes neurons to spend some time as bipolar neurons before they become pyramidal neurons.

These early development stages, might be required in order to extend the scope of the neurons beyond the local area, changing them from interneurons to ones that connect outside the locality.

The question is arising whether injured environment can serve as a area resembles to early developmental tissue. Or that is possible to influence it that way.

It probably depends on how much of developmental tissue management is done by chemical changes that impact the expression of genes, and how much is done by scaffolding of chemicals external to the cell, that it encounters as it grows. If the external scaffolding only existed for a short period of time, during development, and is then lost, simulating it might be much more difficult in an injured environment than hoped.

There might be a case for filling the void with glial cells, that can absorb the neurotransmitter through re-uptake, and thus reduce the neurotoxicity of the area. Because this results wholely from differentiation and doesn't rely on structural growth, it might be an effective strategy.

We have experience with different animal models for the study of neural plasticity. Working with pcd (Purkinje cell degeneration) mice, that lost postnatally most mitral cells in the olfactory bulb, the target of SVZ new neurons, we do not see recovery of affected populations. The system does not seem to respond to neurodegeneration. Happy to provide additional information if useful.

I recently attended a really interesting talk about stem cell transplants in rodents where according to behavioural tests they work quite well in parkinsons, huntingtons and middle artery occlusion.... But in clinical studies there seemed to be a lot of ethical and practical problems so that most of them had to stop

We have published recently a study on stem cell transplants in these same rodents.

Bone Marrow Cell Transplantation Restores Olfaction in the Degenerated

Olfactory Bulb

J. Neurosci. 2012;32: 9053-9058