A few years ago, MIT neuroscientists found that they could dramatically reduce the amyloid plaques that were seen in mice with Alzheimer’s disease simply by showing them light flickering at a specific frequency. Now, a new study has concluded that this flickering light treatment has widespread effects at the cellular level, helping not only neurons, but also immune cells called microglia.

The study found that flickering lights can reduce inflammation, enhance synaptic function, and protect against cell death, in mice that are genetically programmed to develop Alzheimer’s disease.

“It seems that neurodegeneration is largely prevented,” said Li-Huei Tsai, the director of MIT’s Picower Institute for Learning and Memory and the senior author of the study. In addition, the study found that the flickering light boosted cognitive function in the mice, who performed much better on tests of spatial memory than untreated mice did.

In the study, Tsai and her colleagues focused on two different strains of mice that are genetically programmed to develop Alzheimer’s symptoms. One of the strains is known as Tau P301S, and it haas a mutated version of the Tau protein that forms neurofibrillary tangles like those seen in Alzheimer’s patients. The other is called CK-p25, and it can be induced to produce a protein called p25, which causes severe neurodegeneration.

Tsai and her team found that visual stimulation, given one hour a day for three to six weeks, had dramatic effects on neuron degeneration. After the treatment had been done for three weeks, they saw that the Tau P301S mice showed no neuronal degeneration, while the untreated Tau P301S mice had lost 15 to 20 percent of their neurons. On top of that, neurodegeneration was prevented in the CK-p25 mice, which were treated for six weeks.

“I have been working with p25 protein for over 20 years, and I know this is a very neurotoxic protein. We found that the p25 transgene expression levels are exactly the same in treated and untreated mice, but there is no neurodegeneration in the treated mice,” Tsai said. “I haven’t seen anything like that. It’s very shocking.”

These findings could have a dramatic impact over the way that Alzheimer’s is treated in humans.