US scientists used it to increase levels of a chemical which helps brain cells signal to each other.
This signalling is hindered in Alzheimer’s Disease, the journal Nature reported.
The Alzheimer’s Research Trust said the study suggested a way to keep nerve cells in the brain communicating,
Ageing populations in many countries around the world mean that Alzheimer’s disease and other forms of dementia are set to increase.
Researchers at the Gladstone Institute of Neurological Disease in San Francisco believe that boosting the brain chemical, a neurotransmitter called EphB2, could help reduce or even prevent some of the worst effects of the condition.
Their research suggests that the chemical plays an important role in memory, and is depleted in Alzheimer’s patients.
One of the most noticeable features about the brains of Alzheimer’s patients is the build-up of “plaques” of a toxic protein called amyloid. Over time this leads to the death of brain cells.
However, another characteristic of amyloid is its apparent ability to bind directly to EphB2, reducing the amount available to brain cells, which could in part explain the memory symptoms involved.
To test this idea, they used gene therapy experiments to artificially reduce and increase the amount of available EphB2 in the brains of mice.
When levels of the chemical were reduced, healthy mice developed memory symptoms similar to those seen in mice bred to have a condition similar to Alzheimer’s.
Conversely, when the “Alzheimer’s” mice were given gene therapy which boosted levels of EphB2, their memory symptoms disappeared.
Dr Lennart Mucke, who led the study, said that his team had been “thrilled” to find this.
“We think that blocking amyloid proteins from binding to EphB2, and enhancing EphB2 levels or functions with drugs might be of benefit in Alzheimer’s Disease.”
However UK researchers said that the find, while interesting, did not offer a swift answer to Alzheimer’s patients.
Rebecca Wood, chief executive of the Alzheimer’s Research Trust, said: “Our brains are hugely complex and understanding how they work and become damaged by diseases like Alzheimer’s is a massive task.
“This research adds a piece to the Alzheimer’s puzzle and provides new leads for researchers.
“It suggests a way to keep nerve cells in the brain communicating, which is vital for thinking and memory.”
But she added: “We don’t know yet if these findings will lead to a new treatment for Alzheimer’s – that’s some way off.”