The GlucoBrain project uses advanced organ-on-chip technology to link the gut, pancreas, and brain, mapping how diabetes drives dementia and memory loss.
When researchers at Yale gave a shelved cancer drug to old mice whose brains were already riddled with Alzheimer’s-like damage, the animals started remembering again. Synapses that had gone quiet flickered back to life. Proteins that mark healthy brain connections climbed toward normal levels. And when the drug was taken away, the cognitive gains stuck.
The drug is saracatinib, originally developed by AstraZeneca under the code name AZD0530 to treat solid tumors. It never panned out for cancer. But a team led by Stephen Bhatt and Christopher van Dyck at Yale School of Medicine recognized that its molecular target, an enzyme called Fyn kinase, plays a central role in how amyloid-beta destroys synapses in Alzheimer’s disease. Their work, published across several peer-reviewed studies between 2015 and 2020, has made saracatinib one of the more closely watched examples of drug repurposing in neuroscience. As of mid-2026, the compound’s preclinical results remain striking, but its clinical story is more complicated.
Communication begins long before children learn to speak. Researchers at National Yang Ming Chiao Tung University (NYCU) in Taiwan have now uncovered how early brain activity helps build developing communication circuits via regulating FOXP2/Foxp2, a gene linked to human speech and communication disorders.
Published in EMBO Reports, the study presents an integrated framework linking neural activity, vocal circuit development, and activity-dependent regulation of Foxp2 in early life. The researchers studied neonatal mice, which emit ultrasonic vocalizations when separated from their mothers. These vocalizations are widely used to study early social communication and neurodevelopmental disorders.
Using advanced activity tagging, live neural recording, and circuit manipulation techniques, the NYCU team identified a previously underappreciated communication circuit linking the ventromedial prefrontal cortex (vmPFC) and the striatum.
Neurons, the uber-connected nerve cells that act as a main switchboard for the brain, are central to some incredibly complicated processes. They make it possible to think, walk, speak, and breathe. They even have built-in backup batteries to use in emergencies.
Yet the way individual neurons go about their business is surprisingly simple, according to a new Yale study.
How simple? Most of them operate entirely like tiny on-off switches.
For centuries, we’ve assumed that science has banished the transcendent and established that reality is entirely physical. But critics argue there are signs that a rigorous materialism might be holding science back. Increasingly, “emergence” is used to account for everything from consciousness to spacetime – a convenient placeholder for what materialist science may be unable to explain. Physicists like Heisenberg and Hawking concluded that science gives us models of reality, rather than final descriptions of its true nature, while there are scientists working in everything from biology to computer science who suggest that dualism is a productive metaphysical framework for their research. Materialism may have enabled science to reach beyond the dogmas of religion, but there are now those who are restlessly probing the limits of materialism itself.
The other 99% is used on the activity the brain generates on its own: neurons (nerve cells) firing and signalling to each other regardless of whether you’re thinking hard, watching television, dreaming, or simply closing your eyes.
Even in the brain areas dedicated to vision, the visuals coming in through your eyes shape the activity of your neurons less than this internal ongoing action.
In a paper just published in Psychological Review, we argue that our imagination sculpts the images we see in our mind’s eye by carving into this background brain activity. In fact, imagination may have more to do with the brain activity it silences than with the activity it creates.