Researchers believe the discovery of a gene signature in healthy brains could help develop preventative treatments for Alzheimer's disease.

The gene signature echoes the pattern in which Alzheimer's disease spreads through the brain much later in life.

University of Cambridge academics say the findings could help uncover the molecular origins of the devastating disease, and may be used to develop preventative treatments for at-risk individuals well before symptoms appear.

Results, published in the journal Science Advances, identified a specific signature in the regions of the brain which are most vulnerable to Alzheimer's.

They found the body's defence mechanisms against the proteins partly responsible for Alzheimer's are weaker in these areas of the brain.

The results imply that healthy young people with a non-standard form of this specific gene signature may be more likely to develop Alzheimer's in later life, and would most benefit from preventative treatments if and when they are developed for human use.

Earlier this year, the same researchers proposed that "neurostatins" could be taken by healthy individuals to slow or stop the progression of Alzheimer's, in a similar way to how statins are taken to prevent heart disease.

The new research could help identify who would benefit most from taking these in early life.

Although a neurostatin for human use is still quite some time away, a shorter-term benefit of these results may be to breed genetically modified mice or other animals that repeat the full pathology of Alzheimer's, which is the most common way for scientists to understand this or any disease to develop new treatments.

Alzheimer's disease is currently incurable.

Its molecular origins are also unknown, and it is hoped the gene signature research will help explore why certain parts of the brain are more vulnerable than others.

"To answer this question, what we've tried to do is to predict disease progression starting from healthy brains," said senior author Professor Michele Vendruscolo, of the Centre for Misfolding Diseases at Cambridge's Department of Chemistry.

"If we can predict where and when neuronal damage will occur, then we will understand why certain brain tissues are vulnerable, and get a glimpse at the molecular origins of Alzheimer's disease."

Rosie Freer, a PhD student in the Department of Chemistry and the study's lead author, said: "I hope that these results will help drug discovery efforts - that by illuminating the origins of disease vulnerability, there will be clearer targets for those working to cure Alzheimer's disease."