Nature is the key to helping Nerve recovery

(ORDO NEWS) — Researchers at the University of Queensland (UQ) have discovered a molecule needed to regulate the repair process of damaged nerves, which could help people recover from nerve damage.

The discovery was made on the example of the nematode worm C. elegans, which has long been studied by researchers due to its ability to self-repair nerve cells.

Professor Massimo Hilliard and his team at the Queensland Brain Institute (QBI) UQ found that the ADM-4 enzyme is an important protein that regulates the molecular glue, or fusogen, needed for nerve repair.

“We have shown that animals deprived of ADM-4 cannot repair their nerves by fusion,” said Professor Hilliard.

“ADM-4 must function within the damaged neuron to stabilize the EFF-1 fusogen and allow the membranes of the separated nerves to connect.”

“The exciting part of this discovery is that ADM-4 is similar to a mammalian gene, which opens up the possibility that one day we may be able to use this process in humans.”

Nature Is the Key to Helping Nerve Recovery

The study’s first author, Dr. Xue Yan Ho, says the nematode provides an excellent platform for this research.

“Our goal is to identify the molecules and understand their role in nerve repair in C. elegans,” Dr. Ho said. If we can understand how to control this process, we can apply this knowledge to other animal models.”

It is hoped that one day we will be able to induce the same mechanical process in people who have suffered a nerve injury.” “We are still very far from this goal, but the discovery of the role of ADM-4 is an important step forward.”

Nerve cells communicate using long, cable-like structures called axons. Because they are long and thin, they are very prone to tearing, which stops communication between nerve cells and leads to problems such as paralysis.

Gene technology can heal nerve damage

A few years ago, Professor Hilliard and his team discovered that C. elegans can spontaneously join two separated axon fragments, a process called axon fusion.

QBI Associate Professor Victor Anggono helped the team determine the molecular mechanisms behind this process. “The use of neurosurgery to suture damaged nerves has had limited success,” Associate Professor Anggono said.

“Another approach, using gene technology to directly provide the molecular glue, or to activate the ADM-4 fusogen regulator, or using pharmacology to activate these components, could promote complete regeneration.”

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