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Nerve cells generated from stem cells in an adult, diseased, and damaged brain function as normal nerve cells. This has been shown at Lund University in Sweden in a new study published in the prestigious journal Neuron. The new nerve cells also seem to have a positive function, namely, to counteract the disease in the brain.
Until the middle of the 1990s researchers believed that new nerve cells could not be generated in the adult brain. Then it was found to be possible, and that new nerve cells are formed not only in healthy brains but also in brains affected by disease and damage. Professor Olle Lindvall, Assistant Professor Zaal Kokaia, and their associates at Lund University were the first scientists to demonstrate that new nerve cells could be created from the stem cells of an adult brain following a stroke and then migrate to the damaged area.
However, it has been unclear just how these new nerve cells function. Do they behave normally, and are they beneficial or detrimental to a diseased brain? For the first time, Professor Olle Lindvall, Assistant Professor Merab Kokaia, doctoral candidate Katie Jakubs, and others have now managed to answer these questions on the basis of experiments on rats.
"Our study shows that nerve cells that are generated from stem cells in an adult epileptic brain develop into normal nerve cells. Interestingly, they also join up with other nerve cells in a way that indicates they are trying to counteract the diseased function," says Olle Lindvall.
This work, carried out at the Section for Restorative Neurology and the Stem Cell Center at Lund University, is basic research, but it has potential clinical applications down the road. By learning more about how new nerve cells are formed and how they function, it may be possible in the future to help the brain heal itself after a disease or injury.
More information: Olle Lindvall, cell phone: +46 705-171466; e-mail: olle.lindvall@med.lu.se . The article is available at www.neuron.org.
http://www.neuron.org/content/article/abstract?uid=PIIS0896627306008701&high... (abstract)
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