For years, scientists believed that damaged nerve tissue could not be repaired because neurons are incapable of regeneration. But nerve stem cellsimmature precursors that can become neuronsexist in embryos and have recently been found in the adult brain as well. These cells are a potential source of spare neurons that researchers might use to replace damaged brain or spine tissue. To develop new and more effective treatments, however, scientists need to learn more about the molecules regulating the metamorphosis from stem cell to neuron.

To that end, researchers from the University of Milan in Italy report in the June issue of Nature Neuroscience that they have discovered a key signal that makes nerve stem cells transform into mature, functional neurons. Elena Cattaneo and her colleagues found that a small protein called Shc C (pronounced "chic C") was present in mature neurons but not in nerve stem cells. Another protein from the same family, ShcA, existed only in the stem cells, where it is necessary for proliferation. The scientists guessed that the two proteins could have opposite effects. And they were able to show that switching from ShcA to ShcC made nerve stem cells turn into adult neurons. "Regulation of [ShcA and C] availability during brain development may represent the key event that drives proliferative of differentiative signals," the authors wrote.

The regulation of cell changes typically involves many different signaling molecules in a domino-like chainone signal prompts another one and so one. Shc proteins, which have multiple "docking sites" for many types of molecules, can connect different factors in the domino chain, just like a plug travel adaptor. The switch between ShcA and C results, therefore, in different "connector functions," which in turn activate different regulatory proteins affecting the cell's fate. Finding a way to turn this molecular switch on and off would enable scientists to efficiently manipulate neuronal stem cells. "Based on [our] evidence, strategies for interfering with neuronal cell demise in neurodegenerative diseases should include consideration of ShcC levels and activity," the authors say.