Lifeboat Foundation

Summary: As artificial intelligence (AI) evolves, its intersection with neuroscience stirs both anticipation and apprehension. Fears related to AI – loss of control, privacy, and human value – stem from our neural responses to unfamiliar and potentially threatening situations.

We explore how neuroscience helps us understand these fears and suggests ways to address them responsibly. This involves dispelling misconceptions about AI consciousness, establishing ethical frameworks for data privacy, and promoting AI as a collaborator rather than a competitor.

But recently, the nose has gained scientific attention as a gateway to the rest of the body — even the brain, a notoriously difficult target.

The upshot: Someday, inhaling therapies could be as routine as swallowing pills.

The nasal route is quick, needle-free, and user-friendly, and it often requires a smaller dose than other methods, since the drug doesn ’ t have to pass through the digestive tract, losing potency during digestion.

Fatigue is the subjective sensation of weariness, increased sense of effort, or exhaustion and is pervasive in neurologic illnesses. Despite its prevalence, we have a limited understanding of the neurophysiological mechanisms underlying fatigue. The cerebellum, known for its role in motor control and learning, is also involved in perceptual processes. However, the role of the cerebellum in fatigue remains largely unexplored. We performed two experiments to examine whether cerebellar excitability is affected after a fatiguing task and its association with fatigue. Using a crossover design, we assessed cerebellar inhibition (CBI) and perception of fatigue in humans before and after “fatigue” and “control” tasks. Thirty-three participants (16 males, 17 females) performed five isometric pinch trials with their thumb and index finger at 80% maximum voluntary capacity (MVC) until failure (force 40% MVC; fatigue) or at 5% MVC for 30 s (control). We found that reduced CBI after the fatigue task correlated with a milder perception of fatigue. In a follow-up experiment, we investigated the behavioral consequences of reduced CBI after fatigue. We measured CBI, perception of fatigue, and performance during a ballistic goal-directed task before and after the same fatigue and control tasks. We replicated the observation that reduced CBI after the fatigue task correlated with a milder perception of fatigue and found that greater endpoint variability after the fatigue task correlated with reduced CBI. The proportional relation between cerebellar excitability and fatigue indicates a role of the cerebellum in the perception of fatigue, which might come at the expense of motor control.

SIGNIFICANCE STATEMENT Fatigue is one of the most common and debilitating symptoms in neurologic, neuropsychiatric, and chronic illnesses. Despite its epidemiological importance, there is a limited understanding of the neurophysiological mechanisms underlying fatigue. In a series of experiments, we demonstrate that decreased cerebellar excitability relates to lesser physical fatigue perception and worse motor control. These results showcase the role of the cerebellum in fatigue regulation and suggest that fatigue-and performance-related processes might compete for cerebellar resources.

Brain waves act as carriers of information. A recently proposed “Cytoelectric Coupling” hypothesis suggests that these wavering electric fields contribute to the optimization of the brain network’s efficiency and robustness. They do this by influencing the physical configuration of the brain’s molecular framework.

In order to carry out its multifaceted functions, which include thought, the brain operates on various levels. Information like objectives or visuals is depicted through synchronized electrical activity among neuronal networks. Simultaneously, a combination of proteins and other biochemicals within and surrounding each neuron physically execute the mechanics required for participation in these networks.

A new paper by researchers at MIT, City University of London, and Johns Hopkins University posits that the electrical fields of the network influence the physical configuration of neurons’ sub-cellular components to optimize network stability and efficiency, a hypothesis the authors call “Cytoelectric Coupling.”

According to a new study, crows possess the cognitive ability for one of the linguistic elements that make human language so complex.

In the early 2000s, Noam Chomsky and other linguists thought that if there was one thing that belonged specifically to human language, it was recursion, and that this was what distinguished human language from animal communication. As it turns out, this is not the case: a 2020 study proved that rhesus monkeys can do the thing too, and a newly published study shows that crows can also do recursion.

OK, so what’s recursion? It’s the capacity to recognize paired elements in larger sequences – something that has been claimed as one of the key features of human symbolic competence. Consider this example: “The rat the cat chased ran.” Although the phrase is a bit confusing, adult humans easily get that it was the rat that ran and the cat that chased. Recursion is exactly this: pairing the elements “rat” to “ran” and “cat” to “chased”.

The foremost physiological effect of psychedelics in the brain is to significantly reduce activity in multiple brain areas, which contradicts the mainstream reductionist expectation. Physicalist neuroscientists have proposed that an increase in brain noise explains the subjective richness of a psychedelic experience, but a psychedelic experience isn’t akin to TV static, argues Bernardo Kastrup.

Before 2012, the generally accepted wisdom in neuroscience was that psychedelic substances—which lead to unfathomably rich experiential states—stimulate neuronal activity and light up the brain like a Christmas tree. Modern neuroimaging, however, now shows that they do precisely the opposite: the foremost physiological effect of psychedelics in the brain is to significantly reduce activity in multiple brain areas, while increasing it nowhere in the brain beyond measurement error. This has been consistently demonstrated for multiple psychedelic substances (psilocybin, LSD, DMT), with the use of multiple neuroimaging technologies (EEG, MEG, fMRI), and by a variety of different research groups (in Switzerland, Brazil, the United Kingdom, etc.). Neuroscientist Prof. Edward F. Kelly and I published an essay on Scientific American providing an overview of, and references to, many of these studies.

These results contradict the mainstream metaphysics of physicalism for obvious reasons: experience is supposed to be generated by metabolic neuronal activity. A dead person with no metabolism experiences nothing because their brain has no activity. A living person does because their brain does have metabolic activity—or so the story goes. And since neuronal activity supposedly causes experiences, there can be nothing to experience but what can be traced back to patterns of neuronal activity (otherwise, one would have to speak of disembodied experience). Ergo, richer, more intense experience—such as the psychedelic state—should be accompanied by increased activity somewhere in the brain; for it is this increase that supposedly causes the increased richness and intensity of the experience.

A recent study on monkeys found that stimulating a certain part of the forebrain wakes monkeys from anesthesia.

Summary: Treating a mouse model of multiple sclerosis (MS) with the pregnancy hormone estriol could reverse myelin breakdown in the brain’s cortex, a primary area affected in MS.

MS results in inflammation that damage the myelin coating around nerve fibers in the brain’s cortex, leading to disability worsening. Current MS treatments only target inflammation and can’t repair myelin damage.

However, the new study found that estriol not only prevented brain atrophy but also induced remyelination, suggesting it could repair MS-induced damage.

A key challenge in neuroscience is to understand how the brain can adapt to a changing world, even with a relatively static anatomy. The way the brain’s areas are structurally and functionally related to each other—its connectivity—is a key component. In order to explain its dynamics and functions, we also need to add another piece to the puzzle: receptors.

Now, a new mapping by Human Brain Project (HBP) researchers from the Forschungszentrum Jülich (Germany) and Heinrich-Heine-University Düsseldorf (Germany), in collaboration with scientists from the University of Bristol (UK), New York University (U.S.), Child Mind Institute (U.S.), and University of Paris Cité (France) had made advances on our understanding of the distribution of receptors across the brain.

The findings were published in Nature Neuroscience, and the data is now freely available to the neuroscientific community via the HBP’s EBRAINS infrastructure.