Why scientists are betting on light therapy to cure Alzheimer’s: Study finds an hour a day of flashing light STOPPED the disease in mice by thwarting two proteins – as human trials get under way

• The MIT team first announced in 2015 that light therapy stopped Alzheimer’s in mice 
• Now human trials are starting, flashing light into their eyes for an hour a day
• Today, a new study from MIT offered an explanation as to how the therapy works
• They found it targets two types of protein responsible for cell death
• The mice saw cognitive skills such as spatial memory in both mice with dementia and in older, healthy peers 

Hopes are riding on light therapy as a possible cure for Alzheimer’s disease – and a new study suggests there is merit to the radical idea.

In 2015, a neuroscientist in Boston found flickering light shone into the eyes of dementia-suffering mice for one hour a day stopped cell death in their brains by breaking down protein clumps. 

Though the findings were robust, there was widespread skepticism that it could work.

But now, as human trials get under way, the team at MIT has published new research showing how the light therapy works, by targeting the chemical that creates protein clumps, suggesting it may be even more powerful than previously thought.  

‘I haven’t seen anything like that. It is very shocking,’ senior author Dr Li-Huei Tsai, director of the Picower Institute for Learning and Memory at Massachusetts Institute of Technology, said.

The therapy by MIT scientists improved cognitive skills such as spatial memory in both mice with dementia and in older, healthy peers. The team says it should work for humans, too

Previously, Dr Tsai had found that flashes of LED light, shone into the eyes of dementia-suffering mice, destroy the rogue proteins that cause cell death.

However, it wasn’t clear why and how that was happening, leading other experts in the field to question whether this was all just a shot in the dark. 

In the new paper, Dr Tsai’s team attempts to parse out why this is worth our attention.

As the protein clumps broke down, the team recorded improvements in many parts of the brain – strengthening neurons, boosting immune cells, breaking down clumps of protein, and reducing inflammation. 

We still don’t fully understand how dementia takes hold of the brain, and how to curtail it. 

Millions of dollars have been poured into drug trials trying to stop the disease in its tracks by targeting tau proteins (which cause clumps in the brain) and various types of brain cells that seem to be where the disease begins – to no avail. 

Dr Tsai concedes that ‘to be honest, we really don’t know’ where to focus our attention. 

But in this latest study, her team showed that light hampered two types of proteins (tau P301S and CK-p25), and as a result curbed the disease.   

The light therapy started shortly before degeneration would have been expected to begin.

After three weeks, the tau P301S mice were stable, while those untreated had lost up to 20 percent of their neurons.

The CK-p25 mice that saw the light were kept stable for six weeks, while their peers deteriorated.

The therapy improved cognitive skills such as spatial memory in both mice with dementia – and, intriguingly, in older, healthy peers. 

Looking at the brains in autopsy afterwards, they found the disease had been stopped in its track for every mouse that saw the light.

‘It seems neurodegeneration is largely prevented,’ Dr Tsai said. 

This would offer hope preventing the disease in people at risk of developing it. 

Prof Tsai said: ‘I have been working with p25 protein for over 20 years, and I know this is a very neurotoxic protein.

‘We found the p25 transgene expression levels are exactly the same in treated and untreated mice, but there is no neurodegeneration in the treated mice.’

The researchers also found that the treated mice performed better in remembering their way around a water maze. 

Dr Tsai’s original study on the effects of flickering light showed that visual stimulation at a frequency of 40 hertz (cycles per second) induces brain waves known as gamma oscillations in the visual cortex.

These are believed to contribute to normal brain functions such as attention and memory, and previous studies have suggested they are impaired in Alzheimer’s patients.

The researchers later found combining the flickering light with sound stimuli – 40-hertz tones – reduced plaques even more and also had further-reaching effects, extending to the hippocampus and parts of the prefrontal cortex.

They have also found cognitive benefits from both the light- and sound-induced gamma oscillations.

Dr Tsai said: ‘After all, oscillations are initiated by neurons, and I still like to think they are the master regulators.

‘I think the oscillation itself must trigger some intracellular events, right inside neurons, and somehow they are protected.’

The researchers also plan to test the treatment in mice with more advanced symptoms, to see if neuronal degeneration can be reversed after it begins.

Preliminary studies using light and sound stimulation in a small number of patients are underway. 

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