A discovery in a transparent roundworm has brought scientists one step closer to understanding nerve degeneration.
Queensland Brain Institute researchers have discovered the worm contains two proteins that play a role in the degeneration of axons in nerve cells.
Project leader Associate Professor Massimo Hilliard, a group leader at QBI, said axons – long, thread-like nerve cell sections that transmit information – were one of the first parts destroyed in neurodegenerative disease.
“By understanding the molecules involved in axonal degeneration, we can find better ways to protect neurons,” Dr Hilliard said.
“Axons are often hit and damaged by external trauma or internal injury.”
Nerve axons are also damaged in neurodegenerative conditions including Alzheimer’s disease and Parkinson’s disease.
C. elegans a model organism
The researchers discovered the new proteins by using a laser to cut axons in the roundworm Caenorhabditis elegans (C. elegans).
C. elegans is a small organism with only 302 neurons. It was the first multicellular organism to have its genome sequenced and is powerful model organism for neurobiological studies.
Senior author and Monash collaborator Dr Brent Neumann, previously of QBI, said C. elegans is an ideal research model.
“This tiny worm – about 1mm long – allows us to understand what happens in axonal degeneration on a molecular and genetic level,” Dr Neumann said.
“We found there is cross-talk between the dying neuron and the surrounding tissue, where the neuron sends a signal that it needs to be cleaned up.”
The proteins identified seem to alter the membrane of the dying neuron.
Scope to limit nerve degeneration in humans
The study’s co-lead author, Ms Annika Nichols, said the discovery created new avenues for researchers seeking to limit the degenerative process.
“The aim would be to allow neurons to be better preserved,” she said.
“The molecular components we discovered are conserved across evolution, meaning that the same proteins exist in the C. elegans worm as in flies, mice and humans.”
Key collaborators on the project included Professor Ding Xue from the University of Colorado, Boulder, and Professor David Hall from the Albert Einstein College of Medicine, New York.