A major contributor to most neurological diseases is the degeneration of a wire-like part of nerve cells called an axon, which electrically transmits information from one neuron to another. The molecular programs underlying axon degeneration are therefore important targets for therapeutic intervention — the idea being that if axons can be preserved, rather than allowed to die in diseased conditions, then loss of critical processes like movement, speech or memory will be slowed.

For more than 150 years, researchers believed that axons died independently of one another when injured as a result of trauma, such as stroke or brain injury, or of a neurological disease, such as Alzheimer’s.

But a new study challenges this idea and suggests that axons coordinate each other’s destruction, thereby contributing to the degeneration that makes neurological diseases so devastating and permanent.

The paper appears in the journal Current Biology.

The coordination described in the paper creates a ripple effect of neuron death that confounds efforts to restore the growth of healthy cells. However, the researchers also found that the death spiral can be slowed when this communication is blocked using a laboratory method that could inspire pharmacological therapies to treat pathological axon degeneration. The method demonstrates that injured axons can be preserved for at least 10 times longer when their communication with neighbors is blocked.

The researchers believe that axons communicate the death message to each other during injury as a leftover activity, “borrowed” from the nervous system’s developmental period when axons are overproduced and then improper or unnecessary connections are eliminated by similar communication between axons. While this process is essential during development, it appears to be hijacked in diseased or traumatic conditions to reactivate and accelerate neuron degeneration.

The researchers have found that axons receive the message to die as a chemical signal via a cell surface receptor known as “death receptor 6.” They speculate that this chemical signal is released from the axon itself, and they currently are working to determine the identity of this chemical signal.

Paper: “Death Receptor 6 Promotes Wallerian Degeneration in Peripheral Axons”
Reprinted from materials provided by the University of Virginia.

18 Μαΐου, 2017