Not every cell in your brain is a neuron shooting quick signals on their way to deciding whether or not you want bacon on your hamburger (you do). Some of them perform axillary functions that help axons and dendrites send communicate. One type of cell in this category are oligodendrocytes, which insulate axons – the long, pointy parts of neurons – and promote the transmission of signals by creating myelin sheath around them.
Now, keep in mind that every cell in your brain comes from a common ancestor. After all, your body started as a single cell, with the development and directing of stem cells leading to all the different types of cells you know and love. And these precursor cells are told what cells to grow into by protein growth factors called neurotrophins.
Neurotrophins, in turn, work by getting picked up by receptors in the developing cells. So long as both receptors are present and getting fed their neurotrophins, everything is fine and dandy. But if one type of receptor bites the dust, the other one changes roles drastically. In short, if the neurotrophin receptor p75 is left to do its job all on its own, it becomes the destroyer of extremely important oligodendrocytes.
Unfortunately, this is exactly what happens in the case of trauma.
There’s a host of research being conducted on how to regrow nerve cells both within the brain and along the spinal cord. Researchers from Ohio State University, however, took a different route. They decided instead to see what they could do about saving the neurons that are already there, because they continue to die off even after the original injury.
In a recent study, the researchers report a major breakthrough. They’ve discovered an experimental oral drug that turns off the p75 receptors on oligodendrocytes, thus keeping them healthy and alive. And keeping more of these cells alive means keeping an exponential number of nerves alive, because each oligodendrocyte can take care of up to 30 nerve cells.
The experimental drug, called LM11A-31, was tested in mice with spinal cord injuries. The drug was shown to help the survival rate of axons in the nervous system. The placebo group lost 75 percent of them in the lesion area, while those on the drug saw a 50 percent greater survival rate. Plus, those loaded up with the most amounts of the drug – up to 100 milligrams per kilogram of body weight – showed improvements in motor function. They could walk and swim with coordinated leg movements despite their original debilitating injuries.
The results are the first time that an oral drug has ever been shown to improve movement after spinal cord injury independent of any other treatment.
The paper, “Oral Administration of a Small Molecule Targeted to Block proNGF Binding to p75 Promotes Myelin Sparing and Functional Recovery after Spinal Cord Injury,” was published in The Journal of Neuroscience by Ohio State professor of molecular and cellular biology Sung Ok Yoon; Chhavy Tep, Tae Hee Lim, Pyung On Ko, Sami Getahun, Jae Cheon Ryu and Virginia Goettl of the Department of Molecular & Cellular Biochemistry; and Michele Basso of the Department of Physical Therapy, all at Ohio State; and Stephen Massa of the University of California, San Francisco.