Motor neurone disease leads to wasting of the muscles
Scientists have identified a molecule which could be key to understanding the cause of motor neurone disease (MND) and other neurodegenerative disorders.
The Proceedings of the National Academy of Sciences study raises the hope of new treatments being developed.
The London-based team showed the molecule, Wnt3, plays a key role in establishing connections between nerve cells and the muscles they control.
These connections become progressively weaker in MND patients.
Without properly-formed connections - or synapses - the muscle cannot receive the nerve signal that tells it to contract.
This results in the muscle weakness that is typical of MND.
However, scientists have not been clear how synapses are formed in normal circumstances and this has made it very difficult to pin down what goes wrong in MND.
The researchers, from University College London and King's College London, identified Wnt3 as key to the process.
It assists a second molecule, called Agrin, which co-ordinates construction of the connection - or synapse.
Lead researcher Professor Patricia Salinas said: "The work we are publishing today puts an important piece of the puzzle in place and offers up a new possibility for developing drugs to treat MND and other neurodegenerative diseases.
"If we can build up a thorough picture to show how synapses are normally formed between nerves and muscles we can start to look for any elements that aren't working properly in people with MND.
"This might also lead to strategies for nerve repair after an injury."
The team of researchers looked at the function of Wnt signals in chickens, mice and in cells.
In all three cases, it was shown to enhance the effectiveness of Agrin.
Professor Salinas added: "Chickens that don't have the Wnt signal in their developing wings have all of the muscle tissue that we would expect to see, but they don't make strong connections between nerves and muscles.
"So we know that Wnt is definitely affecting synapse formation rather than anything else to do with muscles.
"Now that we understand the role Wnt plays we can begin to explore any role it plays in MND and whether it could be a good target for treating this type of neurodegenerative disease."
Dr Belinda Cupid, of the MND Association, said: "We know from recent research that signs of motor neurone damage, on a cellular level, in models of MND occur very much earlier than the symptoms appear, so any new knowledge of how healthy motor neurones and muscles interact will give us new clues about what might be going wrong in those people affected by this cruel disease."