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A study published in Nature Neuroscience shows that Lemborexant, a medication for insomnia, preserved up to 40% of hippocampal volume and reduced the Tau protein that destroys neurons in Alzheimer’s
A medication for insomnia that millions of people use to sleep may be protecting the brain from something much greater than a bad night’s sleep.
Researchers from the University of Washington in the United States discovered that Lemborexant — marketed as Dayvigo — preserved up to 40% more volume in the hippocampus of mice and significantly reduced levels of the Tau protein, which is primarily responsible for the destruction of neurons in Alzheimer’s.
The study was published on May 27, 2025, in the journal Nature Neuroscience, one of the most respected journals in the world in neuroscience.
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The discovery opens up a possibility that scientists did not expect: a medication for insomnia could slow the progression of Alzheimer’s by decades.
What the insomnia medication does in the brain that surprised scientists
Lemborexant works by blocking orexin — a neuropeptide that keeps the brain alert.
By blocking orexin, the medication helps a person fall asleep naturally, without sedating the entire brain.
What no one expected is that this same blockage would have an extraordinary side effect: the reduction of Tau protein in the brain.
Tau protein is considered the main factor responsible for neurological damage in Alzheimer’s, according to researcher David Holtzman from the University of Washington.
When Tau accumulates abnormally, it forms tangles inside neurons that literally strangle them to death.
This causes the progressive loss of memory, personality, and cognitive ability that defines the disease.
Alzheimer’s affects tens of millions of people worldwide, and to this day, there is no treatment capable of reversing or completely halting the progression of the disease.
40% more preserved hippocampus — what this means in practice
The hippocampus is the region of the brain responsible for forming new memories.
It is the first area attacked by Alzheimer’s — and that is why patients with the disease first lose the ability to remember recent events.
In the study, mice treated with Lemborexant had between 30% and 40% more volume in the hippocampus preserved, compared to groups that received zolpidem — another widely used medication for insomnia — or no medication at all.
To understand the scale: losing 40% of the hippocampus is the difference between recognizing your children and not remembering who they are.
Lemborexant, by preserving this region, could potentially delay the most devastating symptoms of the disease for years or even decades.
In addition to preserving brain volume, the study also showed that genetic deactivation of the orexin 2 receptor caused a similar reduction in Tau levels, reinforcing the link between this system and neurodegeneration.
- Medication: Lemborexant (Dayvigo), approved by the FDA in 2019 for insomnia
- Observed effect: preservation of 30-40% more volume in the hippocampus
- Target protein: Tau — primarily responsible for neurodegeneration in Alzheimer’s
- Publication: Nature Neuroscience, May 27, 2025 (Parhizkar et al.)
- Team: University of Washington (USA)
- Comparison: zolpidem did NOT show the same protective effect
What researchers say about the discovery
“We showed that Lemborexant improves sleep and reduces abnormal tau, which appears to be the main factor responsible for the neurological damage observed in Alzheimer’s,” stated David Holtzman, a researcher at the University of Washington.
In a press release, Holtzman went further: “We need ways to reduce the abnormal accumulation of tau protein and the accompanying inflammation, and it is worth exploring this type of sleep aid further.”
The statement is particularly relevant because it comes from one of the leading Alzheimer’s researchers in the world.
Holtzman is not claiming that Lemborexant cures Alzheimer’s — he is saying that the mechanism deserves urgent investigation in humans.
Lemborexant vs. zolpidem: not all insomnia medications protect the brain
A crucial piece of data from the study is that the protective effect did not appear with just any medication for insomnia.
Zolpidem — probably the most prescribed sleep aid in Brazil — did not show the same preservation of the hippocampus in mice.
The difference lies in the mechanism of action of each medication.
While zolpidem acts on GABA receptors, sedating the brain in a generalized manner, Lemborexant specifically blocks orexin — and it is this selective blockage that seems to have the neuroprotective effect.
This means that sleeping better, by itself, may not be enough to protect against Alzheimer’s.
What matters is how the medication induces sleep and which neurological pathways it activates — or deactivates — in the process.
A parallel study with suvorexant — another orexin blocker, similar to Lemborexant — showed a reduction of 10 to 20% in amyloid levels and 10 to 15% in hyperphosphorylated tau in cerebrospinal fluid from humans, reinforcing that this class of medications deserves special attention.
When Lemborexant will arrive in Brazil
In the United States, Lemborexant was approved by the FDA in 2019 and is marketed as Dayvigo.
In Brazil, the medication has been under review by Anvisa since 2022.
There is still no official timeline for approval, but the publication of the study in Nature Neuroscience may help accelerate the regulatory process.
For Brazilians dealing with insomnia and a family history of Alzheimer’s, the possibility of a single medication addressing both problems is particularly relevant.
The caveats that science insists on highlighting
The study has important limitations that need to be considered before any excessive enthusiasm.
The results were obtained in male mice. The study did not include females, and hormonal differences may significantly alter the effects in humans.
Additionally, Lemborexant is approved only for short-term use in the treatment of insomnia. The effects of continuous and prolonged use — which would be necessary for protection against Alzheimer’s — are still completely unknown.
The mechanism is also indirect. Lemborexant improves sleep and blocks orexin, which reduces Tau. However, direct causality in humans still needs to be proven in controlled clinical trials.
No one should start taking Lemborexant on their own expecting to prevent Alzheimer’s.
Science needs time — but the early signs are promising enough to keep an eye open.
Or better: to keep your eyes closed, sleep well, and perhaps protect your brain while resting.
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