Tooth enamel can begin to dissolve when the mouth’s pH falls below about 5.5. The new findings suggest that sparkling water can temporarily lower oral pH, but the effect appears to be less pronounced than the drop caused by soda.

“Many people are switching from soda to sparkling water, and our findings suggest that unsweetened sparkling water may be a lower-risk alternative to soda, when consumed in moderation and alongside good oral hygiene practices,” said Wajiha Zulfiqar, a graduate student in Nutrition Science at Purdue University.

Zulfiqar presented the results at NUTRITION 2026, the flagship annual meeting of the American Society for Nutrition, held July 25-28 in National Harbor, Maryland, just outside Washington, D.C.

Comparing Sparkling Water and Soda

Previous research has shown that sugar-sweetened soda can promote dental erosion by pushing mouth pH below 5.5. Far less is known about how unsweetened sparkling water influences acidity inside the mouth.

To investigate, researchers tested sugar-sweetened soda, regular sparkling water, calcium-fortified sparkling water, and plain water in 20 adults. Every participant drank each beverage, allowing the team to reduce the influence of natural differences between individuals.

The researchers measured salivary pH rather than relying only on the acidity of the beverages themselves. This allowed them to observe how the mouth responded immediately after each drink was consumed.

“Directly comparing different beverages using the same experimental framework allowed us to evaluate the effects of sparkling water relative to both soda — a higher-risk beverage — and plain water as a neutral reference,” said Zulfiqar. “Additionally, by measuring how the mouth responded in real time, rather than only testing beverage acidity alone as other studies have done, our study provides a more realistic understanding of how these drinks may impact oral health.”

Soda Caused the Largest Drop in pH

Among the beverages tested, soda produced the greatest increase in mouth acidity. Salivary pH was significantly lower after soda than after water at both 2 minutes and 20 minutes following consumption.

Regular unsweetened sparkling water caused a temporary decline in salivary pH after 2 minutes. Calcium-fortified sparkling water produced a decrease after 5 minutes. With both types of sparkling water, pH had returned to nearly its starting level within 20 minutes.

Saliva also helped restore normal acidity after participants drank soda or sparkling water. In the short term, pH remained above the threshold associated with enamel damage.

The researchers emphasized that the experiment measured only brief changes in salivary pH. The likelihood of dental erosion in everyday life can also be affected by how often someone drinks a beverage, how long the teeth are exposed to it, and whether the drink contains sugar.

A Potentially Safer Soda Alternative

“Our results suggest that replacing sugar-sweetened sodas with unsweetened sparkling water may help lower the risk of enamel erosion,” said Zulfiqar. “The results also highlight an opportunity for the beverage industry to explore reformulation strategies that could potentially reduce the erosive potential of acidic beverages.”

The team next plans to examine the long-term effects of sparkling water on oral health. Future studies could determine whether it alters other features of the mouth that contribute to healthy teeth and gums.

Zulfiqar presented the research on Sunday, July 26, during the Clinical Nutrition II Poster Session in the Gaylord National Resort & Convention Center (abstract).

Abstracts presented at NUTRITION 2026 were reviewed and selected by a committee of experts. However, they generally have not completed the peer review process required for publication in a scientific journal. The findings should therefore be regarded as preliminary until they appear in a peer-reviewed publication.

The makeup of those moon systems is very different. Jupiter has four especially large moons, including Ganymede, the biggest moon in the Solar System. Saturn, by comparison, is dominated by Titan, the Solar System’s second largest moon.

A Longstanding Moon Formation Mystery

Because Jupiter and Saturn are both gas giants, astronomers have struggled to explain why their major moons developed so differently. Existing theories of satellite formation offer several possible answers, but recent research into stellar magnetic fields suggests that some of those ideas may need to be reconsidered.

One unresolved question involves magnetic accretion and the formation of satellites. Researchers have debated whether Jupiter’s circumplanetary disk could have developed an empty inner region. A circumplanetary disk is the rotating collection of material around a young planet from which moons can form.

A single physically consistent theory capable of explaining both Jupiter’s and Saturn’s moon systems could also help scientists understand planets and moons outside the Solar System. That possibility led researchers from institutions in Japan and China, including Kyoto University, to create a new model.

“Testing planet formation theory is somewhat difficult because we have only our Solar System for reference, but there are multiple satellite systems close to us whose detailed characteristics we can observe,” says first author Yuri I. Fujii.

Simulating Young Jupiter and Saturn

The researchers used numerical simulations to examine the internal structures and thermal evolution of Jupiter and Saturn when the planets were young. This allowed them to estimate how the planets’ magnetic fields may have changed over time.

They also modeled the circumplanetary disks surrounding both worlds. In addition, the team ran N-body simulations to track the formation of moons and the gradual movement of their orbits. The calculations were carried out using the PC cluster at the Center for Computational Astrophysics, National Astronomical Observatory of Japan.

Jupiter’s Magnetic Field Created a Safe Zone

The simulations indicate that the contrasting moon systems of Jupiter and Saturn may have emerged from differences in the structures of their circumplanetary disks. Those differences, in turn, appear to have been controlled by the strength of each planet’s magnetic field.

Young Jupiter had a powerful magnetic field that created a magnetospheric cavity inside its circumplanetary disk. This inner gap likely helped capture and preserve Io, Europa, and Ganymede as they moved through the disk.

Young Saturn’s magnetic field was not strong enough to create a similar cavity. Without that protected region, migrating moons could not survive inside Saturn’s disk.

Predicting Moon Systems Beyond the Solar System

The findings may help guide future observations of exomoons and the disks surrounding young gas giants. According to the model, planets as large as Jupiter or larger should tend to develop compact systems containing several moons.

Gas planets closer to Saturn’s size, however, may typically end up with only one or two moons.

The researchers now plan to apply their theory to additional moons and to possible exomoon systems around distant planets.

The Soyuz MS-28 spacecraft touched down safely by parachute on July 26 at 5:27 a.m. CDT (3:27 p.m., Kazakhstan time) southeast of Dzhezkazgan. The crew had departed the space station at 2:03 a.m.

Williams and his crewmates spent 241 days in space after launching to the International Space Station on Nov. 27, 2025. During the mission, they completed 3,856 orbits of Earth and traveled more than 102 million miles.

The flight marked the first space mission for Williams and Mikaev. It was Kud-Sverchkov’s second journey into space.

Cancer Research and Advanced Manufacturing

While living aboard the orbiting laboratory, Williams contributed to numerous scientific studies and technology demonstrations. His work included research that could support the development of new cancer treatments.

He also helped investigate ways to improve the production of materials in space for use in high performance computers and electronics.

Williams conducted two spacewalks during the mission. One prepared the station for upgrades to its electrical power system, while the other involved replacing a faulty joint on the Canadarm2 robotic arm.

The crew’s research and maintenance work may benefit people on Earth while also helping NASA prepare for future human exploration of the Moon and Mars.

Recovery and Return to Houston

After completing medical evaluations at the landing site, the crew members will travel by helicopter to Karaganda, Kazakhstan, where recovery teams are stationed.

Williams will then fly aboard a NASA aircraft to the agency’s Johnson Space Center in Houston.

More Than 25 Years of Continuous Human Presence

Astronauts and cosmonauts have continuously lived and worked aboard the International Space Station for more than 25 years. The laboratory allows researchers to conduct experiments and achieve scientific breakthroughs that would not be possible under conditions on Earth.

Research aboard the station helps NASA better understand the demands of human spaceflight, develop solutions for extended missions, and create new commercial opportunities in low Earth orbit.

The station also provides an important foundation for future journeys to the Moon through the Artemis program and, eventually, human missions to Mars.

Too much fat can increase the risk of diabetes, heart disease, and other health problems. Yet the opposite can also be dangerous. In rare genetic and autoimmune conditions such as familial partial lipodystrophy type 2 (FPLD2), abnormal fat loss and uneven fat distribution can also lead to diabetes and other metabolic diseases.

A Longstanding Fat Loss Mystery

Elif Oral, M.D., a clinician and Professor in the Division of Metabolism, Endocrinology and Diabetes, has spent much of her career trying to understand this apparent contradiction. Her goal has been to uncover why pathological fat loss damages metabolism and to improve treatment options for people with lipodystrophy syndromes.

Working with patients who have FPLD2, Oral joined Ormond MacDougald, Ph.D., Professor of Molecular & Integrative Physiology, graduate student researcher Jessica Maung, Ph.D., and a broader collaborative team to investigate what happens inside diseased fat tissue.

“A simple explanation is that all of the fat cells (adipocytes) have really catastrophic things happening in them,” said Maung.

To study the process, the researchers developed a mouse model in which they could switch off the lamin A/C gene specifically in adipocytes. This is the same gene that is mutated in people with FPLD2.

Fat Cells Lose Their Normal Functions

The researchers examined both the animal models and tissue donated by patients. They found major changes in gene activity that prevented fat cells from properly processing and storing lipids.

At the same time, the adipocytes and the immune cells within the fat tissue shifted into a pro-inflammatory state. The mitochondria inside the fat cells also stopped functioning normally. Mitochondria help generate energy for cells, so their failure can have widespread effects on cell health.

Said Maung, “All of these effects come together to create this perfect environment for the tissue to be really unhealthy and eventually disappear.”

Why Healthy Fat Protects Metabolism

When healthy adipose tissue is lost, the body can no longer manage lipids or release metabolic hormones in the usual way. This breakdown can contribute to serious conditions, including diabetes and fatty liver disease.

“This is really underscoring the importance of healthy fats in keeping metabolism intact and functional,” said Oral. “People think of Type 2 diabetes as a disease of beta cells, but it’s actually a disease of fat cells, too.”

Beta cells are the insulin-producing cells in the pancreas. Although they play a central role in diabetes, the new findings show that fat cells are also deeply involved in maintaining normal blood sugar control and metabolic health.

New Targets for Future Treatments

The researchers hope their findings will point to new therapeutic targets. One possibility is to protect adipose tissue before it deteriorates, preventing fat cells from disappearing and reducing the metabolic damage caused by the disease.

The work also highlights the importance of close collaboration between laboratory scientists, clinicians, and patients.

“I think this work is an outstanding example of a collaboration between a translational clinical researcher and a basic science physiologist,” said MacDougald. “We also can’t overstate the importance of the patient population and their involvement in developing therapies and their dedication to understanding their disease.”

Additional authors include Rebecca L. Schill, Akira Nishii, Maria Foss de Freitas, Bonje N. Obua, Marcus Nygård, Maria D. Mendez-Casillas, Isabel D.K. Hermsmeyer, Donatella Gilio, Ozge Besci, Yang Chen, Brian Desrosiers, Rose E. Adler, Anabela D. Gomes, Merve Celik Guler, Hiroyuki Mori, Romina M. Uranga, Ziru Li, Hadla Hariri, Liping Zhang, Anderson de Paula Souza, Keegan S. Hoose, Kenneth T. Lewis, Taryn A. Hetrick, Paul Cederna, Carey N. Lumeng, Susanne Mandrup.

Using donated brain tissue from older adults with and without cognitive decline, along with samples from cognitively healthy centenarians, the team uncovered distinct cellular programs and immune cell states linked to both disease progression and resistance. The findings, published in Nature Medicine, point to changes in microglia, the brain’s resident immune cells, as a potentially important focus for future Alzheimer’s treatments.

“This has been an exciting journey with many partners. The study, entirely based on human donor material, provides insight into one type of resilience mechanism in the progression of AD to dementia,” says Prof. Bart De Strooper (VIB-KU Leuven Center for Neuroscience, KU Leuven), ERC grantee and one of the co-senior authors of the study.

Why Alzheimer’s Pathology Does Not Always Cause Dementia

Alzheimer’s disease affects more than 55 million people worldwide. It is commonly associated with the buildup of amyloid-β plaques and tau tangles in the brain. However, these biological signs do not always match a person’s mental condition.

Some people accumulate substantial amounts of plaques and tangles yet remain cognitively healthy. This has led scientists to focus more closely on how brain cells react to these abnormal proteins, rather than simply measuring how much pathology is present.

Microglia appear to be especially important. These immune cells help monitor and protect the brain, but their behavior can change dramatically as Alzheimer’s advances. By understanding those changes, researchers may be able to explain why some people remain resilient and identify new ways to prevent cognitive decline.

The new findings suggest that people can resist Alzheimer’s related damage through more than one biological pathway. By comparing brain tissue from people with dementia, people without dementia, and cognitively healthy centenarians (people over the age of 100 years), the researchers identified different microglial responses associated with protection from the disease’s effects.

“Understanding better how the brain resists the disease will provide new avenues towards therapies to prevent neurodegeneration and dementia,” adds Prof. Mark Fiers (VIB-KU Leuven), co-senior author of the study.

Mapping a Critical Alzheimer’s Transition

To investigate how resilience develops, the team combined two advanced methods that examine tissue at the level of individual cells (spatial transcriptomics and single-cell sequencing).

These technologies allowed the researchers to identify six distinct tissue domains that appeared to represent different stages of Alzheimer’s progression. One especially important transition separated regions dominated by amyloid-β plaques from those associated with tau pathology and neurodegeneration.

That shift was accompanied by a major change in the behavior of microglia.

During the earlier stages of the disease process, microglia entered an inflammatory state linked to amyloid plaques. At a later stage, they moved into a different antigen-presenting state that appeared at the same time as tau pathology.

Antigen presentation is a process in which immune cells display molecular material to help coordinate an immune response. In this case, the change may mark a biological turning point that helps determine whether Alzheimer’s pathology continues toward brain cell damage and dementia.

Two Biological Paths to Alzheimer’s Resilience

The researchers also found that resilience did not look the same in every person.

Octogenarians who had developed amyloid plaques but remained free of dementia showed the early microglial response. However, their microglia did not move into the later immune state associated with disease progression.

Centenarians followed a different route. Their brains activated the later microglial program, but this response occurred largely without being tied to tau accumulation.

In other words, a cellular state that was associated with neurodegeneration in some people appeared to be separated from damaging effects in others. This suggests that resilience is not simply a matter of avoiding Alzheimer’s pathology. It may also depend on how the brain controls, redirects, or adapts its response to that pathology.

A New Direction for Alzheimer’s Treatment

The results could support the development of more precise Alzheimer’s therapies.

Instead of focusing only on removing amyloid plaques, future treatments might aim to preserve beneficial early microglial activity or influence the transition between different microglial states. Molecules involved in these shifts could become valuable therapeutic targets.

Timing may also be critical. Treatments could be most effective before the brain reaches the point where inflammatory activity becomes connected to tau pathology, neurodegeneration, and cognitive decline.

“These findings open new opportunities to target microglial states — especially pathways such as TREM2 — and extend resilience rather than simply focusing on plaque removal. We are excited to continue this journey and understand the causal role of microglial transitions leading to the identification of novel therapeutic approaches to delay or prevent disease progression,” concludes Niels Plath, CSO of Muna Therapeutics.