A type of protein which helps increase lifespan in yeast and worms could offer hope for new treatments in diseases such as Parkinson's and Alzheimer's.
Around 40% of the C. elegans worm's gene are found in humans
Researchers from Washington School of Medicine say it appears to help prevent damage to nerve cells in the brain which occur in such diseases.
The team say it may be possible to create drug or gene treatments which can mimic this action.
The research is published in the magazine Science.
The scientists, based in St Louis, looked at nerve cells in mice.
They looked at axons, which connect nerve cells to other cells.
In diseases such as Parkinson's and Alzheimer's, it is thought these axons may start to "self-destruct" before the nerve cells actually die.
It was found that a protein called SIRT1 appeared to block some or all of this process.
The effect was confirmed when the scientists administered a drug which shuts down the activity of this type of protein to the nerve cells - and found the protective effect disappeared.
The proteins have previously been linked to extending the lifespan in yeast and the tiny worm C. elegans.
Jeffrey Milbrandt, professor of medicine and of pathology and immunology at the medical school, who led the research, said: "It's becoming clear that nerve cell death in these disorders is often preceded by the degeneration and loss of axons.
"If this mechanism for delaying or preventing axonal degeneration after an injury proves to be something we can activate via genetic or pharmaceutical treatments, then we may be able to use it to delay or inhibit nerve cell death in neurodegenerative diseases."
The researchers said the next step in the research was to look at exactly how SIRT1 delayed axon damage.
In a second study, published online by the British Medical Journal, researchers from the University of Birmingham found a cheap, but rarely used drug could be one of the most effective treatments for Parkinson's Disease.
The team looked at results from 17 separate studies which compared the effectiveness of Selegiline, from a group of drugs called monoamine oxidase type B inhibitors (MAOBIs), with the commonly used drug levodopa and dummy treatments.
Use of Selegiline fell significantly in the UK after a 1995 study showed it was linked to high death rates.
But the scientists who carried out this latest analysis suggest this was probably a chance finding.
They say further long-term studies are needed to provide a conclusive answer.
A spokeswoman for the Parkinson's Disease Society said it supported any investigations into more effective drug treatments for the disease.
She added: "We also welcome the US study into the potential of treatments to slow nerve cell damage.
"Research into therapies and treatments, which may enable the rate of this degeneration to be slowed or even reversed, is a key area of interest."
Professor Clive Ballard, Director of Research at the Alzheimer's Society. added: "Further research holds great potential for developing a novel therapeutic approach for Alzheimer's disease and other diseases involving the death of nerve cells.
"There is however a long way to go before there will be practical applications for people with dementia."