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Thursday, 08 December 2016

Flickering light in eyes could form basis of Alzheimer's treatment, study shows

Written by The Press Association

Flickering light in the eyes could form the basis of a breakthrough Alzheimer's treatment with the potential to halt or even reverse the disease, research has shown.

Extraordinary results from experiments conducted in the US have revealed a close connection between brain waves and a clinical hallmark of the condition.

Using flickering light to synchronise firing of neurons at a specific frequency, the researchers were able to reduce levels of a toxic brain molecule linked to Alzheimer's in mice.

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

The 40 hertz (cycles per second) electrical oscillations not only reduced beta-amyloid formation, but also stimulated immune cells to clear the harmful material from the brain.

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 (MIT), 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."

Michael Sipser, dean of MIT's School of Science, said the results "may herald a breakthrough" in the understanding and treatment of Alzheimer's.

He added: "Our MIT scientists have opened the door to an entirely new direction of research on this brain disorder and the mechanisms that may cause or prevent it. I find it extremely exciting."

Once crucial limitation to the study, published in the journal Nature, is that the flickering light treatment only affected levels of beta-amyloid in the brain's visual cortex.

Future work will investigate whether light therapy can have the same effect in other parts of the brain such as the hippocampus, which is most affected by Alzheimer's.

There is already some evidence that it could. At an earlier stage of the research, the MIT team used a fibre optic light source implanted in the brains of genetically engineered mice to clear beta-amyloid from the hippocampus.

Previous studies had hinted that Alzheimer's patients were less likely than healthy people to display "gamma" brain waves, which range from 25 to 80 hertz.

Gamma oscillations are believed to contribute to normal brain functions such as attention, perception and memory.

Intriguingly, behavioural approaches such as mindfulness meditation have been shown to heighten gamma activity.

The US scientists found that fine-tuning the brain wave stimulation to 40 hertz was vital to success. Other frequencies within the gamma range did not have the same effect.

In the fibre optic experiments, the affected neurons were genetically modified to respond to light.

After an hour of stimulation, levels of beta-amyloid in the hippocampus, the brain's key memory centre, were reduced by up to 50%.

For the flickering light studies the scientists put together a simple device consisting of a strip of LEDs that could be programmed to flash at different frequencies.

An hour of exposure to light flickering at 40 hertz cleared away half the beta-amyloid that had built up in the visual cortex brain regions of mice in the very early stages of Alzheimer's. But the peptide deposits returned to their original levels within 24 hours.

Repeating the treatment for seven days led to a 60% reduction in beta-amyloid load in the visual cortex, proving that the effect could be sustained.

The scientists found that light stimulation increased the activity of genes involved in the function of immune cells called microglia. These cells, specific to the brain and spinal cord, have the job of clearing away potentially harmful material.

Increased microglia activity is believed to be responsible for the loss of beta-amyloid seen in the experiments.

Another major result showed that the treatment also curbed the build up of tau protein "tangles" within brain cells, a second hallmark of Alzheimer's that may follow on from the accumulation of beta-amyloid.

The scientists have set up a company, Cognito Therapeutics, to pursue further tests in humans.

British experts described the findings as "interesting" but cautioned that any potential treatments for human patients were still a long way off.

Dr 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.

Alzheimer's Society research director Dr Doug Brown said: "While there are no immediate implications for people who are living with dementia, the study might well give us a spark for new avenues of research to further explore the relationship between rhythms of electrical activity in the brain and Alzheimer's disease."

Dr Mark Dallas, lecturer in cellular and molecular neuroscience at the University of Reading, said: "As the authors indicate we are some way off using this research as a rationale for new treatments.

"Importantly, we are still no clearer if this modulation of amyloid beta will provide cognitive benefits to patients."

Currently, while some of the symptoms of Alzheimer's can be reduced, no drug exists that can halt or slow down progress of the disease.

Last month the search for an effective Alzheimer's treatment suffered a setback with the failure of a new immunotherapy drug, solanezumab, in a large Phase III trial.

Dr Frances Edwards, a reader in neurophysiology at University College London, said: "This is potentially a very interesting paper and if it is correct it is indeed a very important finding."

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