Benfey et al. find that norepinephrine shifts the visual response selectivity of optic tectal neurons in the Xenopus tadpole to favor threatening loom stimuli over more neutral, randomly drifting dots. Mechanistically, norepinephrine induces radial astrocyte activation and glial release of ATP/adenosine, resulting in reduced excitatory neurotransmission and selectivity shift.
A new electronic implant system can help lab-grown pancreatic cells mature and function properly, potentially providing a basis for novel, cell-based therapies for diabetes. The approach, developed by researchers at the Perelman School of Medicine at the University of Pennsylvania and the School of Engineering and Applied Sciences at Harvard University, incorporates an ultrathin mesh of conductive wires into growing pancreatic tissue, according to a study published in Science.
“The words ‘bionic,’ ‘cybernetic,’ ‘cyborg,’ all of those apply to the device we’ve created,” said Juan Alvarez, Ph.D., an assistant professor of Cell and Developmental Biology. While these terms may sound futuristic, he noted this approach is already in use in the form of deep brain stimulation, which treats neurological conditions.
“What we’re doing is like deep stimulation for the pancreas. Just like pacemakers help the heart keep rhythm, controlled electrical pulses can help pancreatic cells develop and function the way they’re supposed to,” he said.
From the article:
‘The researchers have filed a patent application for the use of the system to measure particle masses with microgram-scale precision from the oscillation frequency. Beyond this, they hope the phenomenon will offer insights into emergent periodic phenomena across timescales in nature: “Your neurons fire at kilohertz, but the pacemaker in your heart hopefully goes about once per second,” explains Grier.’
System could shed light on emergent periodic phenomena in biological systems.
Some brain cells can resist the toxic processes associated with Alzheimer’s disease and other forms of dementia. Scientists have now identified the “cellular hazmat team” that keeps neurons healthy.
Neurodegenerative diseases like dementia are characterized by proteins that aggregate in the brain and kill neurons. Tau proteins are one of the main culprits, but they’re not always villains.
In their functional state, they help to stabilize brain structures and facilitate nutrient transport. But misfolded tau proteins clump together, and a higher degree of clumping indicates more advanced neurodegenerative diseases.
“Working in strict secrecy, a government scientist in Norway built a machine capable of emitting powerful pulses of microwave energy and, in an effort to prove such devices are harmless to humans, in 2024 tested it on himself. He suffered neurological symptoms similar to those of ”Havana syndrome,” the unexplained malady that has struck hundreds of U.S. spies and diplomats around the world.
The bizarre story, described by four people familiar with the events, is the latest wrinkle in the decade-long quest to find the causes of Havana syndrome, whose sufferers experience long-lasting effects including cognitive challenges, dizziness and nausea. The U.S. government calls the events Anomalous Health Incidents (AHIs).
The secret test in Norway has not been previously reported. The Norwegian government told the CIA about the results, two of the people said, prompting at least two visits in 2024 to Norway by Pentagon and White House officials.
The CIA investigated a Norwegian government experiment with a pulsed-energy machine in which a researcher built and tested a ”Havana syndrome” device on himself.
When HHMI Investigator Amita Sehgal started studying sleep 25 years ago, the topic elicited a yawn from most biologists. “In the year 2000, if I had suggested to my department that we hire people working on sleep, they would have laughed at me,” says Sehgal, a molecular biologist and neuroscientist at the University of Pennsylvania. “The thinking was that sleep is not something that neuroscientists do; psychologists study sleep and dreams.” Now, more than two decades later, sleep science has finally woken up.
Biologists around the world are now studying sleep in everything from fruit flies to jellyfish to understand the fundamental molecular and cellular mechanisms that drive slumber and answer the age-old question of why we sleep.
“Sleep is widely conserved across the animal kingdom and so it must have some basic function that is the same across species, and so what is that?” Sehgal says. “We’re finally getting to a point where we are recognizing a few basic principles about sleep.”
Researchers at Washington University School of Medicine in St. Louis have developed a method to predict when someone is likely to develop symptoms of Alzheimer’s disease using a single blood test. In a study published in Nature Medicine, the researchers demonstrated that their models predicted the onset of Alzheimer’s symptoms within a margin of three to four years.
This method could have implications both for clinical trials developing preventive Alzheimer’s treatments and for eventually identifying individuals likely to benefit from these treatments.
More than seven million Americans live with Alzheimer’s disease, with health and long-term care costs for Alzheimer’s and other forms of dementia projected to reach nearly $400 billion in 2025, according to the Alzheimer’s Association. This massive public health burden currently has no cure, but predictive models could help efforts to develop treatments that prevent or slow the onset of Alzheimer’s symptoms.
Traumatic injury is the third leading cause of death in the state of Texas, surpassing strokes, Alzheimer’s disease and diabetes, according to the Centers for Disease Control and Prevention. A massive number of these deaths are the result of uncontrolled bleeding. “Severe blood loss can rapidly lead to hemorrhagic shock,” said Dr. Akhilesh Gaharwar, a biomedical engineering professor at Texas A&M University. “Many patients die within one to two hours of injury. This critical period is often referred to as the ‘golden hour.’”
Gaharwar and his fellow researchers in the biomedical engineering department have found a way to extend this golden hour—using clay.
Gaharwar, Dr. Duncan Maitland and Dr. Taylor Ware are developing a suite of injectable hemostatic bandages —biomedical materials that stop bleeding and promote blood to clot faster. Their research is specifically targeting deep internal bleeding where traditional methods like compression are not possible.
Researchers at UC San Francisco have discovered a mechanism that could explain how exercise improves cognition by shoring up the brain’s protective barrier. With age, the network of blood vessels—called the blood–brain barrier—gets leaky, letting harmful compounds enter the brain. This causes inflammation, which is associated with cognitive decline and is seen in conditions like Alzheimer’s disease. The research is published in the journal Cell.
Six years ago, the team identified a brain-rejuvenating enzyme called GPLD1 that mice produced in their livers when they exercised. But they couldn’t understand how it worked, because it cannot get into the brain.
The new study answers that question. Researchers discovered that GPLD1 was working through another protein called TNAP. As the mice age, the cells that form the blood-brain barrier accumulate TNAP, which makes it leaky. But when mice exercise, their livers produce GPLD1. It travels to the vessels that surround the brain and trims TNAP off the cells.