From the article
“Low-frequency infrasound waves bypass standard sensory receptors to vibrate cochlear support cells, proving that these structural units generate local alternative electric fields that trigger unique, non-linear nerve pathways straight to the human brain.”
Summary: Researchers have demonstrated that the human brain processes low-frequency infrasound using an entirely unique biological mechanism. When acoustic waves drop too low for standard auditory hair cells to register, the energy bypasses them completely, hijacking the inner ear’s structural support cells instead. These support units generate alternative electric fields that fire off unique nerve pathways, explaining why infrasound registers more as a raw physical sensation or internal hum than a standard audible sound.
The Non-Linear Volume Spike: This unique biological pathway explains a well-known acoustic puzzle: when infrasound levels creep up even slightly, the perceived volume escalates at an incredibly rapid, non-linear rate. Small steps in environmental pressure instantly make the sound feel overwhelmingly louder.
“Humans can actually perceive infrasound if the sound level is high enough,” says Carlos Jurado, postdoctoral fellow at the Department of Neuromedicine and Movement Science at the Norwegian University of Science and Technology (NTNU).
Some are more sensitive to low-frequency noise. For example, it can come from ventilation systems, heat pumps, wind turbines, industry, transport, generators or transformers. But this is difficult to measure, because the sound is often perceived more as a hum or physical sensation than more high-frequency sound does.
The International Society for Stem Cell Research (ISSCR) today announced the presentation of new clinical data from the STEM-PD Phase I/II clinical trial at the ISSCR 2026 Annual Meeting. The study reports 12-month outcomes evaluating a cryopreserved, off-the-shelf dopaminergic progenitor cell product derived from human pluripotent stem cells for the treatment of Parkinson’s disease.
The findings provide new insights into the safety, feasibility, and biological activity of stem cell-derived dopaminergic cell transplantation in patients with Parkinson’s disease and represent another important step in the clinical translation of regenerative medicine for neurodegenerative disease.
“These data represent the culmination of decades of research aimed at translating stem cell biology into a clinically viable therapy,” said Malin Parmar, Professor in Cellular Neuroscience at Lund University, Sweden, who presented the findings today at the ISSCR 2026 Annual Meeting. “They demonstrate that a stem cell-derived dopaminergic cell product can be manufactured, delivered, and evaluated within a rigorous clinical trial framework. More broadly, they show that regenerative medicine is moving beyond proof-of-concept and into a stage where stem cell-based therapies are being tested in patients for complex neurodegenerative diseases.”
Iv often thought of this possibility myself.
Working memory is the information we need to access to complete the tasks we’re engaged in right now, and scientists think it may be closely entwined with consciousness.
Some people find it useful to talk through their problems—but language isn’t necessary for logical reasoning, cognitive neuroscientists at MIT’s McGovern Institute for Brain Research say.
In research published in the journal PNAS, researchers led by MIT associate professor of brain and cognitive sciences Evelina Fedorenko have shown that people can perform well on tasks that require logical reasoning even if their language abilities are severely impaired. What’s more, brain imaging shows that language-processing parts of the brain are not called on for logical reasoning.
Philosophers, linguists and cognitive scientists have debated the relationship between language and thought for thousands of years, with many arguing that we use language to think. There are good reasons to suspect a close relationship between logic and language, acknowledges Hope Kean, a postdoctoral researcher and former K. Lisa Yang, Integrative Computational Neuroscience (ICoN) Center graduate fellow in Fedorenko’s lab.
While most current Alzheimer’s treatments focus on beta-amyloid plaques, new research targets early-stage DNA damage and chronic neuroinflammation as critical drivers of the disease. In preclinical mouse models, the drug KCL-286 — a compound already proven safe in human spinal cord injury trials — successfully activated DNA repair genes, healed double-strand DNA breaks in neurons, and significantly reduced neuroinflammation. By addressing these foundational pathological processes, KCL-286 has the potential to slow Alzheimer’s progression rather than merely managing symptoms, offering a promising candidate for early or even asymptomatic intervention. Additionally, the article highlights a separate breakthrough in late-stage care, noting that psilocybin successfully restored speech and motor control in a patient after a decade of battling the disease.
A drug, that has previously been shown to be safe and tolerated by humans, reduces multiple disease-linked features of Alzheimer’s in a mouse model of the disease.
DZNE researchers have uncovered a mechanism that determines why a neuron usually forms a single, long extension called an “axon”—a phenomenon that is fundamental to how our brain functions. Contrary to the common view that external cues drive axon formation, the team of scientists concluded that its growth originates primarily inside the cell. Their work, based on cell cultures and published in the journal Nature with collaborators from other institutions in Germany, Austria and Japan, reveals how a neuron’s structure is remodeled to generate the axon.
Neurons in the brain and spinal cord form a vast network in which each cell receives many inputs but sends output through only a single, long extension: the axon. “If our neurons had multiple axons, this would cause chaos in the brain,” says Frank Bradke, a neurobiologist and research group leader at DZNE. “Nature has therefore found a clever way to make sure that neurons generate only one axon. This applies not only to humans, but across the entire animal kingdom. So, we’re dealing with very fundamental processes that shape the wiring of the brain and nervous system.”
Anxiety disorders affect more than 300 million people globally. Several brain regions have been linked to anxiety, but how these regions connect has been poorly understood. By exploring these connections, scientists at St. Jude Children’s Research Hospital revealed that epinephrine-producing C1 neurons in mice modulate fear and anxiety. They found that while the activity of these neurons was normally temporarily elevated in times of stress, prolonged activation led to heightened anxiety that could last many days. Inhibition of C1 neurons reduced anxiety-like behaviors, suggesting these neurons may be worth exploring as therapeutic targets for anxiety disorders. The findings were published today in Neuron.
Anxiety helps us prepare for future threats, but when it is excessive or persistent, it can significantly affect quality of life. Medications exist to alleviate symptoms but can have off-target effects that might discourage long-term use. By identifying C1 neurons as novel modulators of fear and anxiety, Lindsay Schwarz, Ph.D., Department of Developmental Neurobiology, is hopeful that these cells could serve as a new therapeutic target for anxiety-related disorders.
“C1 neurons appear to promote anxiety without directly affecting autonomic functions,” Schwarz said. “This suggests they may be a better target than broadly affecting signaling across the entire brain and body.”
If you’ve ever been riding a wave of creativity that feels like your brain and someone else’s have been Bluetooth-synced and are now finishing each other’s sentences, both instinctively knowing where the song/screenplay/woodworking project or whatever you’re building should go, then you’ve experienced what scientists call brain synchrony.
As described by a team of researchers publishing their findings as a press release on Eureka Alert, originally published in Trends in Cognitive Sciences, it’s a real phenomenon that’s been observed in laboratories and real-world settings. Now, researchers say it isn’t just measurable, but it can actually be strengthened.
Researchers reviewed a decade of studies involving thousands of people, from regular everyday students to professional artists. Using portable EEG headsets, researchers found that when people are genuinely engaged with one another, their brainwave activity begins to align. Even more interesting, when participants received real-time feedback showing how synchronized they were, that alignment often became even stronger.