Researchers at the University of North Carolina have identified a protein that seems to disappear when an axon (transmitter) in a brain cell is physically damaged. The protein, netrin-1, is reduced when an axon is damaged, leading to a loss of connections between neurons as well as “over-excitement” of the damaged axon. Over-excitement can cause pain as well as further damage or even death to the axon.
Mouse experiments indicate that re-introduction of the protein can reverse the effects of damage.
- Injection of the protein could restore some brain function, especially when damage is relatively recent.
- It might also provide a new path for treatment for individuals suffering from severe pain from TBI.
Either benefit would be a big deal.
Human clinical trials may be sometime in the future, but for sufferers, can’t come too soon.
- Tharkika Nagendran, Rylan S. Larsen, Rebecca L. Bigler, Shawn B. Frost, Benjamin D. Philpot, Randolph J. Nudo, Anne Marion Taylor. Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling. Nature Communications, 2017; 8 (1) DOI: 10.1038/s41467-017-00652-y
University of North Carolina Health Care. “When the brain’s wiring breaks: Key molecular details of a common type of brain injury and a possible new treatment strategy.” ScienceDaily. ScienceDaily, 10 October 2017. <www.sciencedaily.com/releases/2017/10/171010143245.htm>.