A breakthrough using flickering light may provide new hope for Alzheimer's patients.

Scientists were able to reduce levels of a toxic protein linked to the degenerative brain disease in mice by exposing them to flickering light.

Sticky deposits of beta-amyloid peptide are believed to be at the root of the disease, triggering effects that lead to the progressive destruction of brain cells.

In the mice experiments, however, exposure to flickering light stimulated the creatures' brain waves, triggering immune cells which absorbed the sticky amyloid proteins.

Although at an early stage, the new research raises the exciting prospect of a drug-free alternative to tackling Alzheimer's.

Lead scientist Professor Li-Huei Tsai, director of the Picower Institute for Learning and Memory at the Massachusetts Institute of Technology, said: "It's a big 'if', because so many things have been shown to work in mice, only to fail in humans.

"But if humans behave similarly to mice in response to this treatment, I would say the potential is just enormous, because it's so non-invasive, and it's so accessible."

The study, published on Wednesday (Dec 7) in the journal Nature, hinges on the observation that Alzheimer's patients show a loss of synchronised brain activity, known as gamma oscillations, which is linked to attention and memory.

To restore the activity, the scientists first used mice that had been genetically engineered such that the neurons that generate gamma activity in the brain were sensitive to light. The technique, known as optogenetics, allowed the scientists to artificially cause groups of neurons to fire in unison by pulsing light into the brains of the mice, reported the Guardian.

After an hour of stimulation, the researchers found a roughly 50 per cent reduction in the levels of beta amyloid proteins in the hippocampus, the brain's memory centre. Closer inspection showed that the amyloid had been taken up by microglia, the brain's immune cells.

In a healthy brain, microglia act as chemical rubbish collectors, surveying the local environment, clearing up unwanted compounds, but in Alzheimer's these cells can lose this function and switch into an inflammatory state in which they secrete toxic compounds instead. Strengthening gamma oscillations appeared to switch the microglia back into a productive state, said the Guardian.

Next, the scientists showed that gamma oscillations could also be stimulated non-invasively in the visual brain region simply by exposing the mice to a flickering light. At 40Hz the flicker of the light is barely discernible and would be "not offensive at all" for a person to have in the background.

After being given one hour of flickering light each day for a week, the scientists saw a 60 per cent reduction of harmful amyloid plaques in the brains of the mice.

Ed Mann, an associate professor of neuroscience at the University of Oxford, said: "I was surprised, and it's exciting, that such a simple stimulus can target a molecular pathway and have such an effect in an hour."

Questions remain, however, about whether boosting gamma oscillations and sweeping amyloid plaques out of the visual brain region would help with memory, which is centred in the hippocampus, or broader cognitive abilities, said the Guardian.

David Reynolds, chief scientific officer at Alzheimer's Research UK, said: "It is conceivable that changing brain cell rhythms could be a future target for therapies, but researchers will need to explore how light flickering approaches could not only reduce amyloid in the visual area of the brain but in those areas more commonly affected in Alzheimer's."

The authors suggest that it may be possible to take a multi-sensory approach, using a combination of flashing lights and vibrating chairs. Tsai and Ed Boyden, a colleague at MIT and co-author, have started a company called Cognito Therapeutics to pursue tests in humans.

There are 850,000 people with dementia in Britain and this figure is expected to reach 1 million by 2025. Earlier this year, dementia overtook heart disease as the leading cause of death in England and Wales.