There’s something special about the APOE2 variant of the APOE (apolipoprotein E) gene: People who carry it tend to live longer, and they have a lower risk of developing Alzheimer’s disease.
Scientists are still trying to figure out why, and now, they have a new lead.
A team led by researchers at the Buck Institute for Research on Aging in the US set out to answer that question using human stem cell-derived neurons and mouse studies.
Scientists at the Max Planck Florida Institute for Neuroscience (MPFI), in collaboration with ZEISS and MetaCell, have developed a powerful new imaging pipeline called Neuroplex. As described in a paper published in eLife, the technique allows simultaneous monitoring of the activity of up to nine distinct neuronal populations in freely moving mice, dramatically accelerating the pace of scientific exploration into how the brain controls behavior.
For years, neuroscientists linking brain activity to behavior have faced a fundamental limitation: Miniscopes, the tiny head-mounted microscopes used to observe neural activity in behaving animals, could capture neural activity, but couldn’t reliably distinguish more than two different types of brain cells at a time.
“To understand the brain, we need to link patterns of activity in specific neurons to behavior,” stated lead author Dr. Mary Phillips. “We can readily use labels to color-code different populations of neurons, but when using miniscopes to correlate neural activity to behavior, we couldn’t distinguish more than two of these populations. This made it difficult to compare the activity across multiple cell types and circuits to understand how specific circuits regulate behavior.”
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.
