Two licensed drugs have been shown to halt brain degeneration in mice, raising the prospect of a rapid acceleration in the search for a medicine to beat Alzheimer’s disease.

The results, presented on Tuesday at the Alzheimer’s Society annual research conference in Manchester, have been hailed as “hugely promising” because they involve medicines that are already known to be safe and well-tolerated in people – potentially cutting years from the timeline for drugs to reach patients.

Speaking ahead of her presentation, Giovanna Mallucci, professor of clinical neuroscience at the University of Cambridge, said: “It’s really exciting. They’re licensed drugs. This means you’d do a straightforward basic clinical trial on a small group of patients because these are not new compounds, they’re known drugs.”

The scientists have chosen not to name the two drugs, which are currently used for conditions unrelated to dementia, to avoid the possibility of patients seeking to use them ahead of any clinical trial to prove their efficacy.

The findings build on a landmark study two years ago, showing that brain cell death could be halted in mice by switching off a faulty signal in the brain that stops new proteins being produced.

However, the breakthrough relied on a compound that had severe physical side-effects including weight loss and diabetes, making it unsuitable for use in humans. The two drugs were identified after Mallucci’s team screened hundreds of licensed compounds in search for something safe that had the same protective effects on the brain.

Clare Walton, research manager at the Alzheimer’s Society, said: “The new results are hugely promising because the drugs are already given to people and we know they’re safe.”

Before a trial, though, the scientists said that a brain imaging study would be crucial to confirm that the same faulty signal that the drugs target in mice is responsible for neurodegeneration and the devastating memory loss it causes in Alzheimer’s.

“There is lots of evidence that points to the pathway being involved, but we need to do special scanning to show that what’s happening to the mice is happening to humans,” said Mallucci. “The big, burning question is what is the relevance for human disease.”

If scanning experiments take place quickly, and they confirm a link, clinical trials of the medicines could begin within a couple of years, she added.

The approach marks a clear shift away from previous failed attempts to cure Alzheimer’s by targeting the deposits of misshapen, sticky proteins, known as plaques, that are the most visible hallmarks of the disease in the brains of patients.

“There have been a lot of drug failures in the past decade of things that just targeted the plaques,” said Walton. “Some of the drugs cleared away the plaques but didn’t help treat the disease.”

The latest research suggests that the build-up of abnormal amyloid proteins seen in Alzheimer’s, Parkinson’s and CJD are simply a visible symptom of neurodegeneration, but not the root cause.

Instead, Prof Mallucci argues, the damage really occurs when a natural defence mechanism in the brain responds to the accumulation of plaques by switching off the production of all new proteins, wrecking the brain’s ability to carry out essential repairs.

The drugs work by inhibiting an enzyme, called Perk, that activates the defence mechanism. In mice with prion disease, a neurodegenerative disorder that scientists use as a model for dementia in mice, both treatments were shown to restore protein production, stop brain cells from dying off and prevent memory loss.

There is already evidence that the Perk mechanism plays a role in Alzheimer’s, as people with the disease are known to have unusually high levels of the enzyme in their brains, but scientists need to be confident that this is causing neurons to die rather than just being a side effect.

Carol Colton, a professor of neurology at Duke University in North Carolina, said the results were “exciting”, but added that critical questions remained about whether switching off a natural defence mechanism might have other unforeseen downsides in the brain.

“Time will tell,” she said. “It would be a great thing if possible and new drugs are badly needed. Kudos to the authors and the Alzheimer’s Society for moving this concept along.”

It is estimated at about 820,000 people in the UK have dementia. Scientists estimate that delaying the onset of Alzheimer’s by five years would halve the number of people who die with the disease.

“I have people in my clinics who come in with quality of life and are still able to converse, but over time they become dependent, unable to enjoy the company of their lifetime partners and that’s heartbreaking,” said Mallucci.

“Even delaying progress of Alzheimer’s by 10 years would have a massive effect. You have to re-adjust and understand that slowing Alzheimer’s would change the disease into something completely different and infinitely more acceptable to society.”