Sleeping while listening to bursts of pink noise 鈥� background sounds akin to gentle radio static 鈥� seems to boost the flow of fluid through the brain, and so might enhance the clearance of waste products that are linked to conditions like Alzheimer鈥檚 disease. The pink noise seems to bolster the slow brainwaves that enhance the pumping of blood vessels, which drives the brain鈥檚 waste-disposal system.

We already knew that listening to bursts of pink noise during sleep , a kind of electrical activity that occurs during certain phases of聽non-REM聽sleep, known as聽N3 (deep sleep) and N2 (the lighter stage before it). This effect occurs when the bursts coincide with the peaks of slow brainwaves.

鈥淭hey really don鈥檛 sound like much, they鈥檙e just little staticky beeps,鈥� says at Boston University in Massachusetts.

Prior research has also shown that boosting slow brainwaves 鈥� using drugs, for instance 鈥� can enhance the flow of the brain鈥檚 cerebrospinal fluid (CSF), which bathes the brain and carries away waste products.

But it was unknown whether listening to pink noise has the same effect. That鈥檚 because measuring the brain鈥檚 CSF flow involves imaging it with MRI scans, but MRI interferes with EEG, the technique used to measure waves of electrical activity in the brain. One consequence of this interference is that slow waves recorded via EEG during MRI scans can鈥檛 be detected fast enough to align bursts of pink noise with their peaks.

鈥淵ou have to do a lot of extensive processing of the EEG signals to detect slow brainwaves, so it鈥檚 hard to do that fast enough in real-time,鈥� says at the Massachusetts Institute of Technology.

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To overcome this problem, Levitt, Lewis and their colleagues used EEG data collected during MRI scans from prior studies to train an AI model to rapidly predict when the brain鈥檚 slow waves will peak. 鈥淸The AI] says, 鈥業n about 70 milliseconds, a slow wave peak is coming,鈥� so now we should schedule our sound stimulation to arrive in accordance with that,鈥� says Levitt.

鈥淭his, methodologically, really moves the field forward,鈥� says at the University of New Mexico.

The researchers then recruited 27 healthy adults, aged 29 on average, to wear EEG electrodes on their scalp while taking an afternoon nap in an MRI scanner. Of these, 14 managed to fall asleep and enter N2 sleep. 鈥淚t鈥檚 a difficult place to fall asleep,鈥� says Lewis.

At the peak of half of each participant鈥檚 slow brainwaves, the researchers used the AI model to play 50-millisecond bursts of pink noise. During the remaining slow brainwaves, they played no noise as a control.

By analysing the MRI and EEG recordings, they found that bursts of pink noise strengthened the slow waves they coincided with and briefly boosted the flow of CSF into the brain, compared with no sonic stimulation. This suggests the pink noise also enhanced the flow of CSF through, and out of, the brain. 鈥淲e know that the flow in is usually balanced with the flow that comes out,鈥� says Lewis.

The increased CSF flow seemed to be driven by enhanced pumping of the brain鈥檚 blood vessels, which is known to push fluid through the brain鈥檚 waste-disposal system, called the glymphatic system.

Off the back of these results, the team is exploring whether the approach also works in older adults and whether it can boost the clearance of proteins, such as beta-amyloid, that are linked to conditions like Alzheimer鈥檚 disease. If the results are positive, the researchers hope to test whether the technique can slow cognitive decline in people during normal ageing, mild cognitive impairment 鈥� a condition that often precedes dementia 鈥� and the early stages of Alzheimer鈥檚 disease.

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There is reason to think this could work. Exposing people to sounds and flickering lights 鈥� while they are awake 鈥� has previously shown promise at slowing cognitive decline in people with Alzheimer鈥檚, potentially by boosting the glymphatic system.

But one benefit of the new approach is that it could eventually be delivered via a portable device while people are sleeping, which could be less disruptive, says Ryman.

Neurons have been created from a different type of brain cell that usually supports them. Nerve cell death is a hallmark of Alzheimer鈥檚 disease, but a cage of nanoparticles containing antibodies converted astrocytes, another type of brain cell, into neurons in mice with a version of the condition. This boosted the mice鈥檚 cognitive skills. The researchers behind the approach hope to test it in people in the next few years.

鈥淲e can replace lost neurons and also reverse Alzheimer鈥檚 disease progression [in mice],鈥� says at the University of South Carolina.

In Alzheimer鈥檚 disease, which , the proteins beta-amyloid and tau misfold and form clumps, known as plaques and tangles. This leads to neuroinflammation and, ultimately, nerve cell death.

Researchers are increasingly exploring whether stimulating the growth of new neurons could treat Alzheimer鈥檚 disease and other neurodegenerative conditions. For instance, in 2020, scientists discovered that astrocytes 鈥� star-shaped cells that help neurons function 鈥� in the brains of mice with a version of Parkinson鈥檚 disease, which improved their motor skills.

This involved using CRISPR to genetically engineer the mice to deplete levels of a protein called PTBP1. This usually acts like a master switch that stops astrocytes from turning into neurons.

But such genetic approaches can alter regions of the genome you didn鈥檛 intend to target. 鈥淵ou can sometimes cut the wrong places, causing permanent genetic changes that may be harmful,鈥� says Xu.

To address this issue, he and his colleagues have developed another way to deplete PTBP1. They designed a drug called TN-PTBP1 that packages PTBP1-targeting antibodies within a cage of nanoparticles that shuttles them across the blood-brain barrier.

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The drug enters cells in the brain, including astrocytes, where the antibodies bind to and substantially deplete PTBP1. After about a week, the antibodies are recycled by the cell, says Xu.

The team has now tested this in brain organoids made up of clumps of astrocytes and neurons, which were grown from human stem cells in a lab dish. This showed that TN-PTBP1 converts astrocytes into neurons.

Next, the researchers tried the approach in 12 mice that had been genetically engineered to develop a condition mimicking Alzheimer鈥檚. Prior to receiving TN-PTBP1, brain imaging revealed that these mice had lost a substantial number of neurons, similar to what is seen in moderate-to-severe Alzheimer鈥檚 disease, says Xu. The mice struggled to build nests and performed poorly in a memory test that involved navigating a maze.

The team intravenously injected half of the mice with TN-PTBP1 twice over two weeks, while the rest received saline injections. Two weeks later, the mice that received TN-PTBP1 were able to nest and navigate the maze at a similar level to another group of mice without the version of Alzheimer鈥檚, while the saline group showed no change. 鈥淭here鈥檚 clearly an improvement, which is very thought-provoking,鈥� says at the University of Cambridge.

When the researchers analysed samples of the mice鈥檚 hippocampi, an area of the brain involved in memory and learning, they found that TN-PTBP1 had caused new neurons to sprout in the brain. 聽

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They are now planning more studies in mice where astrocytes are labelled with fluorescent tags to track whether TN-PTBP1 is really behind those cells converting into neurons, says Xu. The researchers also hope to test the approach in monkeys and people in the next few years, he says.

The mice showed no signs of side effects, but future work should explore whether the newly formed neurons safely integrate into the brain鈥檚 networks without disrupting their function over the long term, says at King鈥檚 College London. 鈥淲e need to check [whether] these neurons [would] be beneficial, rather than screwing up the network.鈥�

But with proper testing, the potential of this drug could be huge, he says. It 鈥渃ould have an enormous effect on the treatment of many brain diseases鈥�, including schizophrenia, motor neuron disease (such as ALS) and Parkinson鈥檚 disease, he says.