This gene stops nerve fibers from decaying

"This study demonstrates that mec-17 normally functions to protect the nervous system from damage. This knowledge can now be used to understand precisely how the gene achieves this and to discover other molecules that are used by the nervous system for similar protective functions," says Brent Neumann. (Credit: The Journal of Cell Biology/Flickr)

Scientists have identified a gene that protects against spontaneous nerve degeneration, a discovery that could have implications for treating a range of conditions, including Parkinson’s, Alzheimer’s, and Huntington’s diseases.

“This is an important step to fully understand how axonal degeneration occurs, and thus facilitates development of therapies to prevent or halt this damaging biological event,” says Massimo Hilliard of the Queensland Brain Institute at the University of Queensland.

A new study published in Cell Reports shows that the gene protects the neuron by stabilizing its cytoskeletal structure, allowing proper transport of essential molecules and organelles, including mitochondria, throughout the axon.

The finding also has the potential to accelerate the identification of human neurodegenerative conditions caused by mutations in genes similar to mec-17, Hilliard says.

“It’s our hope that this could one day lead to more effective treatments for patients suffering from conditions causing neuronal degeneration.”

Protect the nervous system

The discovery highlights the axon as a major focal point for the health of the neuron, says lead author Brent Neumann.

“This study demonstrates that mec-17 normally functions to protect the nervous system from damage. This knowledge can now be used to understand precisely how the gene achieves this and to discover other molecules that are used by the nervous system for similar protective functions.

“We can now start to look into means of bypassing the function of mec-17, such as activating other genes or alternative mechanisms that can protect the nervous system from damage.”

Previous research has shown that mec-17 is conserved across species, including humans, suggesting a possible shared function of protection.

“We identified mec-17 from a genetic screening method aimed at identifying molecules that cause axonal degeneration when they become inactive through genetic mutations,” Neumann says.

The research was conducted in the tiny nematode worm C. elegans and funded by the National Health and Medical Research Council and an Australian Research Council Future Fellowship.

Source: University of Queensland