Thursday, March 26, 2026

 

Dreams may make sleep feel deeper, even when the brain is more active



New research suggests that vivid dreaming helps sustain the subjective feeling of deep sleep across the night, offering a new perspective on what shapes our perception of sleep depth.




IMT School for Advanced Studies Lucca

The Sleep Lab 

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Illustration of the research setting where the study was conducted.  

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Credit: Valentina Elce




The feeling of having had “a good night’s sleep” lies not only in how much we slept, but also in the subjective impression of having slept deeply and without interruption. But what constitutes the neural base of this perception is not very well understood.

Now, a new study by researchers at the IMT School for Advanced Studies Lucca, appeared in Plos Biology, suggests that the dreams, especially the most vivid and immersive ones, rather than disrupting sleep, could help it feel deeper and restoring.

For years, we thought deep sleep meant a "switched off" brain: slow brain waves, little activity, no awareness. In this view, the deeper the sleep, the less active the brain. On the other hand, dreaming has been instead associated with Rapid Eye Movement (REM) sleep and it is acknowledged to reflect partial “awakenings” of the brain. Yet, surprisingly, this stage marked by intense dreaming and wake-like brain activity is also commonly experienced as a relatively deep sleep.

To investigate this paradox, researchers analyzed 196 overnight recordings from 44 healthy adults who slept in a laboratory while their brain activity was measured with high-density electroencephalography (EEG). The data were collected in a larger study supported by a European Research Council (ERC) Starting Grant investigating how various kinds of sensory stimulations impact on the subjective experience of sleep.

 

Dreaming changes how brain activity relates to sleep depth

Across four laboratory nights per participant, the researchers collected more than 1,000 awakenings with corresponding reports, creating one of the largest datasets linking brain activity, dream experience, and subjective sleep perception. For the experiment, participants were awakened repeatedly from non-REM sleep, a stage characterized by broad variability in both subjective sleep depth and dreaming, and asked to report their mental experiences just before awakening, and to rate perceived sleep depth and subjective sleepiness.

The results revealed that the deepest subjective sleep was reported not only when participants had no conscious experience, but also after vivid and immersive dreams. By contrast, minimal or fragmentary experiences, such as a vague sense of presence without clear dream content, were associated with the shallowest perceived sleep. “In other words, not all mental activity during sleep feels the same: the quality of the experience, especially how immersive it is, appears to be crucial” explains Giulio Bernardiprofessor in neuroscience at the IMT School and senior author of the study. “This suggests that dreaming may reshape how brain activity is interpreted by the sleeper: the more immersive the dream, the deeper the sleep feels”.

The authors also found another striking element: although physiological markers of sleep pressure steadily decreased across the night, participants paradoxically reported feeling that their sleep was becoming deeper. This subjective deepening closely tracked a rise in the immersiveness of dreams, suggesting that dream experiences may help sustain the feeling of deep sleep even as the biological drive for sleep wanes. Indeed, immersive dreams may help maintain our sense of disconnection from the external world, a defining feature of restorative sleep, even as parts of the brain become more active.

 

Dreams as “guardians of sleep”

“Understanding how dreams contribute to the feeling of deep sleep opens new perspectives on sleep health and mental well-being,” says Bernardi. “If dreams help sustain the feeling of deep sleep, then alterations in dreaming could partly explain why some people feel they sleep poorly even when standard objective sleep indices appear normal. Rather than being merely a by-product of sleep, immersive dreams may help buffer fluctuations in brain activity and sustain the subjective experience of being deeply asleep”. This idea echoes a long-standing hypothesis in sleep research - and even in classical psychoanalysis - that dreams may act as “guardians of sleep.”

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The study was conducted within a broader collaboration between the IMT School, Scuola Superiore Sant’Anna in Pisa, and Fondazione Gabriele Monasterio, where a new  sleep laboratory has been established to bring together complementary neuroscientific and medical perspectives. The laboratory provides a multidisciplinary framework for investigating sleep and the sleep–wake cycle from multiple angles, allowing researchers to more comprehensively explore the interaction between brain activity and bodily physiology. The present findings represent an important first step in this direction and lay the groundwork for future studies examining how brain–body dynamics shape sleep in both physiological and pathological conditions.

 

Scientists discover new genetic disease that causes premature aging and cognitive deficits




Study implicates a surprising gene, shows how its mutation affects cells and identifies a potential treatment




Sanford Burnham Prebys

Brain organoids 

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The scientists studied brain organoids derived from patients suffering from a newly discovered genetic disease. These organoids had a more disorganized structure and fewer properly patterned developing nerve cells than healthy controls, suggesting impaired brain development.

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Credit: Fang Yuan, Su-Chun Zhang, Sanford Burnham Prebys.





Scientists at Sanford Burnham Prebys Medical Discovery Institute and an international team of collaborators have defined a new genetic disease marked by premature aging and deficits in brain function.

The researchers published results on March 19, 2026, in Nature Communications that describe the first known project to combine genome sequencing with cellular reprogramming to identify which gene mutation is at fault and study how it causes the symptoms observed in patients suffering from this newly discovered disease.

“Our collaborator identified a family of patients whose teenaged members had whitening hairs and other characteristics associated with premature aging conditions known as progeria syndromes,” said senior and corresponding author Su-Chun Zhang, MD, PhD, the Jeanne and Gary Herberger Leadership Chair in Neuroscience and the director of and professor in the Center for Neurologic Diseases at Sanford Burnham Prebys.

“Cognitive functions are often well-preserved in these conditions, however, so it was clear from the patients’ progressive loss of motor skills and neurological and intellectual deficits that this was an unknown disease.”

The research team used both genome sequencing and a method for mapping recessive traits to trace the disease to a surprising spot within these patients’ DNA. The investigators implicated a mutation in the IVNS1ABP gene, which holds the instructional codes for building IVNS1ABP, an influenza virus non-structural protein-1 binding protein.

“Relatively little research has been done on this gene and protein, and no one has ever linked them to the biology of aging, premature aging diseases or neuropathy,” said Fang Yuan, PhD, staff scientist at Sanford Burnham Prebys and first author of the study.

“It was a mystery in many ways, and one we were determined to solve.”

To explore the effects of this gene mutation, the scientists acquired samples of skin cells from the affected patients and reprogrammed them into induced pluripotent stem cells. These cells were coaxed into a state that is more mature than a stem cell but not yet a neuron or other brain or nerve cell.

These precursor cells—known as neural progenitor cells—retain the patients’ mutation in the IVNS1ABP gene, enabling experiments to understand what changes it causes on the cellular level.

“Under the microscope, we found that the patient-derived cells with the mutation grow much slower compared to the control group reprogrammed from a sibling without the disease,” said Zhang.

This lethargic growth suggested that the cells had entered a zombie-like state called cellular senescence. Damage to DNA often causes cells to become senescent. When the research team looked at markers of genetic harm, they found three different indicators of injury to the genome, as well as an increased expression level of a cell cycle inhibitor gene associated with cellular senescence called CDKN2A.  

“To narrow in on what was causing these cells to become senescent, we ran follow-up experiments showing that DNA damage was occurring during cell division, and we saw that it could be severe enough to cause cell death,” said Yuan.

Because the mutated gene had no known direct link to cell division, the investigators hypothesized that their observation may be due to interactions between multiple proteins. Their experiments compiled a list of 14 potential proteins that may be involved. Ten of them were connected to actin, one of the structural components that gives shape and structure to a cell.

“During cell division, the actin filament needs to form an anchoring structure, and it usually forms a very round and even ring structure,” said Zhang. “But in the mutant cells, the altered actin forms a shrunken and irregularly shaped ring, so cells are not pulled apart in a symmetrical way and suffer damage.”

The scientists suspected that the mutation was affecting how the cell precisely coordinates the dynamic process of building this actin anchoring structure.

“When these actin dynamics are altered, the cell cannot perform cell division at the right time and in the right place,” said Yuan.

The research team demonstrated that mutant cells had altered actin dynamics, and that the cells could be treated with chemicals to stabilize the actin structure and improve the rate of normal cell division.

“This research highlights the potential of using cellular reprogramming and patient-derived stem cell models to study rare and unknown diseases,” said Zhang.

“And we already showed that if we correct some of the steps in the molecular processes, then we can fix some of the defects, at least in the cellular model,” said Yuan.

“It will be important to complement these findings with studies in an animal model we’re developing, but what we’ve done already demonstrates that this approach is a powerful tool for defining new diseases and developing potential treatments.”

 

Additional authors include:

  • Ye Sing Tan, Qiang Yuan, Shu-Min Chou, Yu-Hsin Yen and Gunaseelan Narayanan from Duke-National University of Singapore (NUS) Medical School
  • Haofei Wang from The University of North Carolina at Chapel Hill
  • Ain Nur Ali, Carine Bonnard and Bruno Reversade from the Agency for Science, Technology and Research in Singapore
  • Lei Zhou from The Hong Kong Polytechnic University
  • Mohammad Shboul from Jordan University of Science and Technology

The study was supported by the National Medical Research Council of Singapore, National Research Foundation of Singapore, Singapore Ministry of Education Research Fund, Singapore Ministry of Health Research Fund, Agency for Science, Technology and Research, Duke-NUS Medical School, European Molecular Biology Organization, Branco Weiss Foundation and Strategic Positioning Fund for Genetic Orphan Diseases.

The study’s DOI is 10.1038/s41467-026-70756-x.