Researchers at Washington University in St. Louis are working on a possible solution. A team led by Gang Wu, professor of energy, environmental & chemical engineering in the McKelvey School of Engineering, has developed a new catalyst designed for an anion-exchange membrane water electrolyzer (AEMWE). This technology uses electricity from renewable sources to split water into hydrogen and oxygen, producing clean hydrogen fuel in the process.

New Platinum-Free Hydrogen Catalyst

Wu’s group focused on replacing expensive platinum-based materials commonly used in hydrogen production systems. Their approach uses renewable electricity generated from sunlight, wind, or water to power the separation of hydrogen from water molecules.

“Going from water to hydrogen is a very desirable way we are able to store energy for different applications,” Wu said. “Hydrogen itself can be used as an energy carrier and is useful for different chemical industries and manufacturing.”

To build the catalyst, the researchers combined rhenium phosphide (Re₂P) and molybdenum phosphide (MoP). Together, the two materials created a highly effective composite that improved the hydrogen extraction process. The rhenium component helped hydrogen attach to and release from the catalyst surface, while the molybdenum sped up the splitting of water in the alkaline electrolyte.

Durable Performance for Clean Energy

The team paired the new catalyst with a nickel iron anode and found that the system performed better than a leading state-of-the-art cathode, including one based on PGM materials. According to Wu, the catalyst also operated for more than 1,000 hours at industry-level current densities of 1 and 2 amperes per square centimeter. That makes it one of the most durable platinum-free cathodes developed so far for anion-exchange membrane water electrolyzers.

“Our findings allowed us to rationalize the critical role of engineering the hydrogen-bond network at the catalyst/electrolyte interface in designing high-efficiency, low-cost AEMWEs,” Wu said. “Our catalyst showed the lowest resistance across the studied potential range, which suggests the fastest hydrogen adsorption kinetics among the studied catalysts. This newly achieved performance and durability metrics make our catalyst one of the most promising membrane electrode assemblies for practical anion-exchange membrane water electrolyzers.”

Potential for Large-Scale Hydrogen Production

Although the experiments were carried out at laboratory scale, the researchers plan to continue studying whether the technology can be expanded for industrial use.

The work was financially supported by G. Wu’s startup fund at Washington University in St. Louis.

In a study published in Nature Neuroscience, researchers from Inserm and the University of Bordeaux at the NeuroCentre Magendie, working with scientists at the Université de Moncton in Canada, reported a major step forward in understanding dementia. Their results showed a direct cause and effect link between faulty mitochondrial activity and cognitive symptoms associated with neurodegenerative disease.

Brain Energy and Memory Loss

The team created a highly specific tool that allowed them to temporarily increase mitochondrial activity in animal models of neurodegenerative disease. When they boosted the brain’s energy machinery, memory problems improved.

Although the findings are still early and were observed in animal models, they point to an intriguing possibility: mitochondria may not simply break down after brain disease begins. Instead, their failure may help drive the symptoms that appear as dementia develops.

That idea could reshape how scientists think about future treatments. If brain cell energy failure contributes to memory loss, then restoring mitochondrial function may one day become a strategy for slowing or reducing symptoms.

Why Mitochondria Matter in the Brain

A mitochondrion is a small structure inside the cell that helps generate the energy required for normal function. This matters especially in the brain, which consumes a large amount of the body’s energy.

Neurons depend on that energy to send signals to one another. When mitochondrial activity drops, neurons may no longer have enough power to work properly. Over time, that energy shortage could weaken communication in the brain and contribute to memory and thinking problems.

Neurodegenerative diseases involve the gradual decline of neuronal function, followed by the death of brain cells. In Alzheimer’s disease, researchers have long observed that mitochondrial problems appear alongside neuronal degeneration, often before cells die. Until recently, however, it was difficult to determine whether mitochondrial dysfunction helped cause the disease process or merely appeared as a result of it.

A Tool Designed to Recharge Mitochondria

To explore that question, the researchers developed a tool that can temporarily stimulate mitochondrial activity. Their reasoning was simple but powerful. If increasing mitochondrial activity improved symptoms in animals, that would suggest mitochondrial impairment can come before neuron loss and contribute directly to cognitive decline.

Earlier work by the research teams had already identified a role for G proteins, which have the specific role of enabling the transfer of information within cells, in regulating mitochondrial activity in the brain. In the 2025 study, they built an artificial receptor called mitoDreadd-Gs. This receptor was designed to activate G proteins directly inside mitochondria, which in turn stimulated mitochondrial activity.

When mitoDreadd-Gs was activated in the brain, mitochondrial activity returned to normal levels. Memory performance also improved in mouse models of dementia.

A Possible New Target for Dementia Research

“This work is the first to establish a cause-and-effect link between mitochondrial dysfunction and symptoms related to neurodegenerative diseases, suggesting that impaired mitochondrial activity could be at the origin of the onset of neuronal degeneration,” explains Giovanni Marsicano, Inserm research director and co-senior author of the study.

The results do not mean that a treatment is ready for patients. The work was performed in animal models, and much more research is needed to determine whether similar approaches could be safe, durable, and effective in humans.

Still, the findings add momentum to a growing shift in dementia research. Scientists are increasingly looking beyond the familiar hallmarks of Alzheimer’s disease, such as amyloid plaques and tau tangles, to examine how energy production, metabolism, inflammation, and cellular stress may shape the disease from its earliest stages.

Recent research has continued to strengthen that broader view. A recent Mayo Clinic study linked disruptions in mitochondrial complex I, a key part of the cell’s energy system, to Alzheimer’s disease progression and potential treatment response. Reviews published afterward have also described mitochondrial failure as an early and potentially central feature of Alzheimer’s biology, not merely a late consequence of brain damage.

“These results will need to be extended, but they allow us to better understand the important role of mitochondria in the proper functioning of our brain. Ultimately, the tool we developed could help us identify the molecular and cellular mechanisms responsible for dementia and facilitate the development of effective therapeutic targets,” explains Étienne Hébert Chatelain, professor at the Université de Moncton and co-senior author of the study.

What Comes Next

The next major question is whether longer term stimulation of mitochondrial activity can do more than improve memory symptoms. Researchers now want to know whether restoring mitochondrial function could slow neuron loss, delay disease progression, or possibly help prevent damage before it becomes irreversible.

“Our work now consists of trying to measure the effects of continuous stimulation of mitochondrial activity to see whether it impacts the symptoms of neurodegenerative diseases and, ultimately, delays neuronal loss or even prevents it if mitochondrial activity is restored,” added Luigi Bellocchio, Inserm researcher and co-senior author of the study.

For now, the discovery offers a striking message: memory loss may be tied not only to dying brain cells, but also to living neurons that are running short on energy. By learning how to recharge those tiny engines, scientists may be opening a new path in the fight against dementia.

The discovery offers a rare direct look at one of the largest structures in existence and could help researchers better understand how galaxies grow and evolve over cosmic time.

The Universe’s Hidden Structure

Modern cosmology suggests that dark matter makes up roughly 85% of all matter in the Universe. Although invisible, dark matter is believed to shape a gigantic web-like framework made of long filaments. At the points where these filaments intersect, galaxies form and shine brightly.

Scientists think these filaments also act as intergalactic highways, channeling gas into galaxies and fueling the birth of new stars. Learning how this gas moves through the cosmic web is considered essential for understanding how galaxies develop.

But detecting that gas has been extremely difficult. Most intergalactic gas has only been observed indirectly by measuring how it absorbs light from bright objects behind it. Hydrogen, the most abundant element in the cosmos, emits only a very faint glow, making direct observations nearly impossible for older instruments.

Hundreds of Hours of Telescope Observations

The new observations were carried out by researchers from the University of Milano-Bicocca together with scientists from the Max Planck Institute for Astrophysics (MPA). The team used MUSE (Multi-Unit Spectroscopic Explorer), a powerful instrument mounted on the European Southern Observatory’s Very Large Telescope in Chile.

Even with such advanced technology, the project required one of the most ambitious MUSE observing campaigns ever conducted in a single region of the sky. Researchers gathered data over hundreds of hours to detect the faint filament clearly enough for detailed analysis.

The study, led by Davide Tornotti, PhD student at the University of Milano-Bicocca, produced the sharpest image ever captured of a cosmic filament stretching roughly 3 million light-years. The structure connects two galaxies that each contain an active supermassive black hole.

The findings were published in Nature Astronomy and provide a new way to study the physical properties of gas inside intergalactic filaments.

A 12-Billion-Year Journey Across Space

“By capturing the faint light emitted by this filament, which traveled for just under 12 billion years to reach Earth, we were able to precisely characterize its shape,” explains Davide Tornotti. “For the first time, we could trace the boundary between the gas residing in galaxies and the material contained within the cosmic web through direct measurements.”

To better interpret the observations, the researchers compared the data with supercomputer simulations of the Universe created at MPA. These simulations predicted what such filamentary structures should look like under current cosmological models.

“When comparing to the novel high-definition image of the cosmic web, we find substantial agreement between current theory and observations,” Tornotti adds.

New Clues About Galaxy Formation

The successful match between observations and simulations gives scientists greater confidence in their understanding of how gas is distributed around galaxies and how galaxies receive the material needed to continue forming stars.

Researchers now hope to identify many more of these faint structures in order to build a broader picture of how matter flows through the cosmic web.

Fabrizio Arrigoni Battaia, MPA staff scientist involved in the study, concludes: “We are thrilled by this direct, high-definition observation of a cosmic filament. But as people say in Bavaria: ‘Eine ist keine’ — one doesn’t count. So we are gathering further data to uncover more such structures, with the ultimate goal to have a comprehensive vision of how gas is distributed and flows in the cosmic web.”

Research from UC Davis Health found that people diagnosed with anxiety disorders had lower levels of choline in the brain than people without anxiety. The finding comes from a study published in Molecular Psychiatry, a Nature journal, and offers a rare look at the chemistry that may be connected to anxiety across several different diagnoses.

The researchers reviewed data from 25 previous studies that measured neurometabolites, the chemicals involved in brain metabolism. Altogether, the analysis included 370 people with anxiety disorders and 342 people without anxiety.

A Consistent Chemical Signal in the Brain

The standout finding was choline. People with anxiety disorders had about 8% lower levels of this nutrient in the brain compared with those in the control groups. The pattern was especially clear in the prefrontal cortex, a brain region that helps regulate thought, emotion, decision making, and behavior.

“This is the first meta-analysis to show a chemical pattern in the brain in anxiety disorders,” said Jason Smucny, co-author and an assistant professor in the Department of Psychiatry and Behavioral Sciences. “It suggests nutritional approaches — like appropriate choline supplementation — may help restore brain chemistry and improve outcomes for patients.”

Choline (pronounced kō-lēn) plays several important roles in the body. It helps form cell membranes and supports brain functions involved in memory, mood regulation, and muscle control. Although the body can make a small amount on its own, most choline must come from food.

Why Anxiety Disorders Matter

Anxiety disorders are among the most common mental health conditions in the United States. Richard Maddock, senior author of the study, is a psychiatrist and research professor in the Department of Psychiatry and Behavioral Sciences. He is also a researcher at the UC Davis Imaging Research Center, where scientists use magnetic resonance imaging (MRI) methods to study brain health.

Maddock has spent decades treating people with anxiety disorders and studying how these conditions affect the brain.

“Anxiety disorders are the most common mental illness in the United States, affecting about 30% of adults. They can be debilitating for people, and many people do not receive adequate treatment,” Maddock said.

Anxiety disorders include generalized anxiety disorder, panic disorder, social anxiety disorders, and phobias.

How the Brain Processes Fear and Stress

Anxiety disorders are connected to the way the brain responds to stress, danger, and uncertainty. Two key regions are often involved: the amygdala, which helps shape the sense of safety or threat, and the prefrontal cortex, which supports planning, decision making, and emotional control.

When this system is working well, the brain can usually separate manageable problems from serious threats. In anxiety disorders, that balance can shift. Everyday concerns may feel overwhelming, and the body’s stress response can become difficult to calm.

Brain chemistry also plays a role. Anxiety disorders have been linked to changes in neurotransmitters, including norepinephrine, which is part of the body’s “fight-or-flight” response. Norepinephrine is often elevated in anxiety disorders, and the UC Davis researchers suggest that this heightened arousal may increase the brain’s demand for choline.

In generalized anxiety disorder, for example, people may worry excessively about ordinary events and struggle to control nervousness or fear.

Measuring Brain Chemicals Without Surgery

Maddock and Smucny have long studied how brain chemistry is connected to mental illness using proton magnetic resonance spectroscopy, also known as 1H-MRS.

This technique is noninvasive and is performed with an MRI machine. Instead of producing a standard image of brain structure, 1H-MRS uses magnetic fields and radio waves to measure chemical levels in tissue.

Maddock had previously seen low choline levels in studies of people with panic disorder. That earlier work helped lead to the larger meta-analysis with Smucny. Even though the researchers expected to see reduced choline, the consistency of the result stood out.

“An 8% lower amount doesn’t sound like that much, but in the brain it’s significant,” Maddock said.

The study also found reduced levels of cortical NAA across brain regions after some exclusions. NAA is often considered a marker related to neuronal health and function. However, the clearest and most consistent signal was the reduction in choline-containing compounds across anxiety disorders.

Choline, Diet, and Mental Health

The researchers think that chronic fight-or-flight activity may raise the brain’s need for choline. If the brain cannot take in enough to meet that demand, choline levels may drop.

That does not mean choline supplements are a proven treatment for anxiety. Maddock emphasized that the question remains open.

“We don’t know yet if increasing choline in the diet will help reduce anxiety. More research will be needed,” Maddock said. He cautions that people with anxiety should not self-medicate with excessive choline supplements.

Still, the finding adds to growing interest in the relationship between nutrition and mental health. Choline is already known to be important for the brain and nervous system, and many people in the United States do not get the recommended daily amount.

“Someone with an anxiety disorder might want to look at their diet and see whether they are getting the recommended daily amount of choline. Previous research has shown that most people in the U.S., including children, don’t get the recommended daily amount,” Maddock said. “Some forms of omega-3 fatty acids, like those found in salmon, may be especially good sources for supplying choline to the brain.”

What Later Research Adds

Since the UC Davis work was published, the broader research picture has remained intriguing but not settled. Related dietary research in adults has suggested that higher choline intake may be linked with lower odds of depression, but the same study did not find a significant adjusted association with anxiety or psychological distress.

That makes the UC Davis brain imaging result especially interesting. It points to a measurable chemical difference inside the brain, but it does not prove that low dietary choline causes anxiety or that increasing choline will relieve symptoms. Controlled trials would be needed to test whether changing choline intake can alter brain chemistry or improve anxiety outcomes.

For now, the findings support a practical but cautious message: nutrition may be one piece of the anxiety puzzle, but it is not a substitute for professional mental health care.

Foods That Provide Choline

Choline is found in several common foods. Rich sources include beef liver, eggs (particularly the yolk), beef, chicken, fish, soybeans and milk, among others.

The study highlights a possible biological link between anxiety and a nutrient the brain depends on every day. It also raises a larger question for future research: whether improving choline status could help restore brain chemistry in people with anxiety disorders.

For now, researchers say the answer is not yet known. But the discovery gives scientists a clearer chemical target to investigate and gives people another reason to pay attention to the nutrients that support brain health.