In what could one day be a landmark study for multiple sclerosis patients, researchers have been able to use human stem cells to not only repair spinal cord injuries in mice (surprise!), but also to spawn oligodendrocytes that then produced the insulating layer of myelin. This is of course important to the MS world because the body's attack on myelin is considered to be the direct cause of multiple sclerosis symptoms, and ultimately, disease progression.
This unique and fascinating study proceeded as follows:
Researchers first gathered fetal neural stem cells, a type of stem cell that is slightly more developed than the usual "blank slate" embryonic stem cells (since they have already become destined to make cells for the central nervous system). On an aside, note that the use of fetal cells is unfortunately bound to be controversial.
The mice "patients" then had their spinal cords "injured" and could no longer walk normally. One should take a moment here to thank these unwitting participants.
Nine days later, some of the mice were injected with the human neural stem cells. Note that the mice were specially bred to not reject human tissue.
After four months, the treated mice could walk normally again, while the untreated mice had not regained their walking abilities!
In a clever twist, the researchers wanted to be sure it was the actual neural stem cells that were causing the improvement, and not some side factor in the mouse itself that was simply invoked in the presence of the stem cells. To do this, they injected the mice with a toxin known to kill human cells but leave mouse cells alone. The result: the mice lost the ability to walk again, indicating that the human neural stem cells were entirely responsible for the restoration of walking ability.
Finally, the cords themselves were analyzed, and the researchers were surprised to see that most of the neural stem cells had formed oligodendrocytes, the myelin "factories" that coat nerve central nervous system axons, providing protection and signal conduction. Again, in MS, a loss of myelin is the most obvious component of the disease.
As usual, more research must be done before testing in humans. The worry is that it is not clear when to inject the stem cells to initaite repair (more of a concern for random spinal injuries as opposed to constant MS attacks on the myelin), as well as how to handle the immune system's potential rejection of foreign stem cells (remember the mice were specifically bred to not reject human cells).
To that end, lead researcher Aileen Anderson noted, "The last thing we want to do is take someone who's living a productive life — if confined, we all understand that — and make them worse...The exciting part is the potential is there." (as quoted by by Lauran Neergaard of the Associated Press).
This is truly a very exciting discovery that though distant in clinical applications, sets the stage for the possibilty that myelin repair is attainable using technology that exists today.
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