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Category: neuroscience

Brain dynamics of the « wave of death » highlighted for the first time

In 2023, scientists at the Paris Brain Institute investigated one of the most fascinating and unsettling transitions in neuroscience: what happens to the cortex when the brain is deprived of oxygen.

In a rat model of systemic anoxia, researchers found that the dying brain does not simply “shut off” all at once. Instead, cortical activity follows a structured sequence: brief high-frequency activity, slowing oscillations, electrical silence, and then a massive wave of anoxic depolarization — often called the “wave of death.”

This wave appeared to begin deep in the neocortex, especially around layer 5 pyramidal neurons, before spreading upward toward the cortical surface and downward toward the white matter. These neurons are large, metabolically demanding projection cells, which may make them especially vulnerable when oxygen and ATP collapse.

But the most important part of the study is that this wave did not always represent an absolute point of no return. When oxygenation was restored within a critical window, researchers observed a “wave of resuscitation,” followed by partial recovery of synaptic activity.

That does not mean death has been “reversed” in a simple or sensational sense. But it does suggest something scientifically powerful: the boundary between life and death in the brain may be more dynamic, layered, and measurable than we often imagine.

This is where the implications become fascinating.

If the “wave of death” is an organized biophysical event, future neurocritical care may one day be able to detect the brain’s approach toward irreversible injury in real time. Instead of relying only on broad markers like heartbeat, oxygen saturation, or flat EEG, clinicians may eventually use more detailed brain-state monitoring to identify whether the cortex is entering a reversible, borderline, or irreversible phase.

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Instant digital rewards may make hard thinking feel less worthwhile

Imagine opening a difficult book in a quiet room. The first page is dense. You read one paragraph, then reread it. Nothing “clicks” yet. Your brain is doing what learning often requires: spending effort before the reward arrives. Then your phone lights up. One thumb movement, and the situation changes completely. A joke, a message, a clip, a tiny social reward: all available instantly, all requiring almost no effort. The book has not become harder and, definitely, your intelligence has not disappeared. But the book now feels more expensive, because another activity nearby offers a much better bargain: reward now, effort almost zero.

That is the central idea of the paper “An Effort Recalibration Framework for Digital Media Use and Cognition” that just appeared in Nature Human Behavior. It argues that the most important effect of social media might be that repeated exposure to effortless digital rewards changes how we value effort itself. Over time, the authors suggest, digital media may recalibrate our internal sense of what effort is worth. Difficult work then begins to feel less attractive, not because we can no longer do it, but because our everyday decision system has learned to expect faster returns.

Explore consciousness theories and implications

It is because the phantom primal eye is centrally evoked by the cellular as generic APS identically with all the contents of special sense information that Leibniz’s “like can only interact with like” condition is satisfied by the non-physical primal eye “monad”—as opposed to Descartes’s cellular pineal gland.

A global hub for theories of consciousness—authenticated by leading theorists, designed for professional consciousness communities, and open to all.

The circuit that lets your brain think and see

Nuttida Rungratsameetaweemana is challenging a story neuroscience has told for decades. According to the conventional account, our eyes collect raw information and relay it through a series of nerves and waystations that lead deep into the brain, eventually reaching the cortex. There, the thinking begins as information is processed and put to use for higher tasks such as reasoning, judgment and decision-making.

Her group’s work is complicating that account. Last year, the team published fMRI scans showing unexpected levels of activity in the earliest visual areas of the cortex, the regions that first receive visual signals. Rather than passively relaying what the eyes take in, those early areas seemed to process the same information differently depending on what the research participant was doing. When asked to sort shapes by one set of rules, a participant’s early visual system behaved one way. When asked to apply a different set of rules to the same shape, it behaved differently.

In a new paper published today in PLOS Biology, Rungratsameetaweemana and her team at Columbia Engineering show how the brain might pull this off. They built a simple neural network that follows many of the rules that govern real brains. Like the brain, their model contained one class of neurons that drive other neurons to fire and another class that suppress firing.

Cognitive flexibility problems may arise months before memory impairment in Alzheimer’s

When most people think about Alzheimer’s disease, memory loss is usually the first thing that comes to mind. Forgetting a loved one’s name, missing appointments or repeatedly misplacing everyday items are often considered early warning signs. But what if the disease begins affecting the brain long before memory problems become noticeable? New research from scientists at Texas A&M Health suggests that another change in brain function may appear even earlier: difficulty adapting when circumstances change.

In a recent study published in Nature Communications, researchers found that animal models with Alzheimer’s-related brain changes developed problems with cognitive flexibility months before they showed signs of memory impairment. Cognitive flexibility refers to the brain’s ability to adjust behavior, learn new rules and adapt when situations change.

“We found that this function was impaired before we could detect deficits in spatial memory,” said neuroscientist Jun Wang, Ph.D., professor in the Texas A&M University Naresh K. Vashisht College of Medicine at Texas A&M Health.

Fear-learning circuit shows how stress disrupts brain’s ability to suppress trauma

Fear is often thought of as a negative emotion but is actually a natural protective response to perceived threats or danger. It helps us survive. When we experience a situation that causes fear, it becomes stored in our brain as a fear memory. These fear memories prevent us from touching a hot stove after being burned or from stepping onto a busy street.

What about fear memories that take over? Post-traumatic stress disorder, or PTSD, is caused by severe acute or chronic stress that disrupts the learning process designed to suppress fear memories. These memories then begin to negatively affect a person’s quality of life.

Typically, our fear memories can be suppressed through extinction learning. The original memory or fear isn’t forgotten, but a new memory is formed and suppresses the original fear memory. However, extinction learning can become tricky in situations that involve traumatic memories.

Trisomic rescue via allele-specific multiple chromosome cleavage using CRISPR-Cas9 in trisomy 21 cells

Human trisomy 21, responsible for Down syndrome, is the most prevalent genetic cause of cognitive impairment and remains a key focus for prenatal and preimplantation diagnosis. However, research directed toward eliminating supernumerary chromosomes from trisomic cells is limited. The present study demonstrates that allele-specific multiple chromosome cleavage by clustered regularly interspaced palindromic repeats Cas9 can achieve trisomy rescue by eliminating the target chromosome from human trisomy 21 induced pluripotent stem cells and fibroblasts. Unlike previously reported allele-nonspecific strategies, we have developed a comprehensive allele-specific (AS) Cas9 target sequence extraction method that efficiently removes the target chromosome. The temporary knockdown of DNA damage response genes increases the chromosome loss rate, while chromosomal rescue reversibly restores gene signatures and ameliorates cellular phenotypes. Additionally, this strategy proves effective in differentiated, nondividing cells. We anticipate that an AS approach will lay the groundwork for more sophisticated medical interventions targeting trisomy 21.

Keywords: CRISPR/Cas; Down syndrome; allele specificity; chromosome cut; chromosome loss; human trisomy 21.

© The Author(s) 2025. Published by Oxford University Press on behalf of National Academy of Sciences.

Consciousness likely not unique to earthlings, paper says

Does consciousness depend on flesh and blood?

The answer is almost certainly no, according to Eric Schwitzgebel, a distinguished professor of philosophy at the University of California, Riverside.

In a new working paper, Schwitzgebel and Jeremy Pober, a former UCR graduate student who is now a postdoctoral researcher at the University of Lisbon, assert that consciousness is likely possible in life forms made of much different stuff. Think of the five-limbed alien with a rock-like exterior in the recent blockbuster movie “Project Hail Mary.”

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