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Electrophysiological correlates of lucid dreaming: sensor and source level signatures

Lucid dreaming (LD) is a state of conscious awareness of the ongoing oneiric state, predominantly linked to REM sleep. Progress in understanding its neurobiological basis has been hindered by small sample sizes, diverse EEG setups, and artifacts like saccadic eye movements. To address these challenges in the characterization of the electrophysiological correlates of LD, we introduced an adaptive multi-stage preprocessing pipeline, applied to human data (male and female) pooled across laboratories, allowing us to explore sensor-and source-level markers of LD. We observed that, while sensor-level differences between LD and non-lucid REM sleep were minimal, mixed-frequency analysis revealed broad low-alpha to gamma power reductions during LD compared to wakefulness. Source-level analyses showed significant beta power (12−30 Hz) reductions in right central and parietal areas, including the temporo-parietal junction, during LD. Moreover, functional connectivity in the alpha band (8−12 Hz) increased during LD compared to non-lucid REM sleep. During initial LD eye signaling compared to baseline, source-level gamma1 power (30−36 Hz) increased in right temporo-occipital regions, including the right precuneus. Finally, functional connectivity analysis revealed increased inter-hemispheric and inter-regional gamma1 connectivity during LD, reflecting widespread network engagement. These results suggest that distinct source-level power and connectivity patterns characterize the dynamic neural processes underlying LD, including shifts in network communication and regional activation that may underlie the specific changes in perception, memory processing, self-awareness, and cognitive control. Taken together, these findings illuminate the electrophysiological correlates of LD, laying the groundwork for decoding the mechanisms of this intriguing state of consciousness.

Significance statement Lucid dreaming (LD) is a unique state of oneiric awareness, where individuals recognize they are dreaming while still in the dream. LD neural correlates remain elusive, as it is very rare and difficult to reproduce in the laboratory. Using an advanced preprocessing pipeline, we harmonized diverse EEG datasets to analyze the largest LD sample to date. We observed gamma power increases in the precuneus during initial eye lucidity signaling, beta power reductions in parietal areas, including the temporo-parietal junction, and enhanced alpha and gamma connectivity during LD over non-lucid REM sleep. These findings shed light on how the brain generates self-referential awareness and volitional action even during sleep.

Scientists discover how to reactivate cancer’s molecular ‘kill switch’

Alternative RNA splicing is like a movie editor cutting and rearranging scenes from the same footage to create different versions of a film. By selecting which scenes to keep and which to leave out, the editor can produce a drama, a comedy, or even a thriller—all from the same raw material. Similarly, cells splice RNA in different ways to produce a variety of proteins from a single gene, fine-tuning their function based on need. However, when cancer rewrites the script, this process goes awry, fueling tumor growth and survival.

In a recent study reported in the Feb. 15 issue of Nature Communications, scientists from The Jackson Laboratory (JAX) and UConn Health not only show how cancer hijacks this tightly regulated splicing and rearranging of RNA but also introduce a potential therapeutic strategy that could slow or even shrink aggressive and hard-to-treat tumors. This discovery could transform how we treat aggressive cancers, such as and certain , where current treatment options are limited.

At the heart of this work, led by Olga Anczuków, an associate professor at JAX and co-program leader at the NCI-designated JAX Cancer Center, are tiny genetic elements called poison exons, nature’s own “off switch” for protein production. When these exons are included in an RNA message, they trigger its destruction before a protein can be made—preventing harmful cellular activity. In , poison exons regulate the levels of key proteins, keeping the genetic machinery in check. But in cancer, this safety mechanism often fails.

Our brains can communicate wordlessly, through our eyes

McGill researchers have demonstrated something long assumed: that glances can transmit information about one’s mental state to others without a single word being exchanged. They speculate that this primal ability may have played a role in assuring the survival of human society at times when making a sound could have attracted predators.

The research is published in the journal Communications Psychology.

“Humans have a long history of living in complex groups and . It has been theorized that this has led our brains to develop a heightened ability to focus on social cues from faces, and especially from eyes,” said Jelena Ristic, a professor in McGill’s psychology department. She has been working in the field for over 20 years. “It’s a system that has evolved to support very quick exchanges of complex social information.”

Watching our brains remember multiple things at once

A new study offers insight into what is happening in our brains when our working memory must use its limited resources to remember multiple things.

Researchers found that two parts of the brain work together to ensure that more brain resources are given to remember a priority item when a person is juggling more than one item in memory.

The study involved people remembering spatial locations. Imagine seeing two books on different shelves of a cluttered bookcase that was not arranged in any order. How could you remember where they were if you came back a few seconds later?

New research points out a promising strategy for treating metastatic medulloblastoma

Researchers at Baylor College of Medicine, Texas Children’s Hospital, the Hospital for Sick Children in Toronto and collaborating institutions reveal in Nature Cell Biology a strategy that helps medulloblastoma, the most prevalent malignant brain tumor in children, spread and grow on the leptomeninges, the membranes surrounding the brain and spinal cord.

They discovered a novel line of communication between metastatic medulloblastoma and leptomeningeal fibroblasts that mediates recruitment and reprogramming of the latter to support tumor growth. The findings suggest that disrupting this communication offers a potential opportunity to treat this devastating disease.

“Metastases, the spreading of a tumor away from its original site, are the most common and most important cause of illness and death for children with medulloblastoma,” said co-first author Dr. Namal Abeysundara, a postdoctoral fellow who was working in the lab of Dr. Michael D. Taylor at the Arthur and Sonia Labatt Brain Tumor Research Center and the Developmental and Stem Cell Biology Program at the Hospital for Sick Children in Toronto, Canada during this project.

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