The mystery became an ideal research question for a master’s student. Clemens Ries, who had recently joined the Max Planck Institute of Psychiatry for an internship as he approached the end of his biology degree, took on the challenge.

Identifying the Brain’s Repair Cells

Using a mouse model, Ries systematically tested markers for all known cell types. Only one produced a response: the marker for oligodendrocyte progenitor cells (OPCs).

These precursor cells can mature into oligodendrocytes, which produce the myelin sheath surrounding axons. Axons are extensions of nerve cells that allow neurons to communicate with one another. Myelin acts much like the insulating material around an electrical cable. It supports efficient information transmission along axons and also helps supply them with nutrients, making it vital to healthy brain function.

Damage to myelin can have serious consequences. In autoimmune diseases such as multiple sclerosis (MS), the protective coating breaks down. Physical injuries can also harm myelin, and in severe cases, the resulting damage can lead to the death of entire neurons. Restoring myelin around affected axons is therefore an important part of the brain’s response to injury.

A Surprising Stress Hormone Appears After Injury

Ries initially studied the newly identified cells for his master’s thesis. “The topic remained so exciting that it became my doctoral thesis,” says the biologist.

His subsequent research showed that these precursor cells multiply dramatically around the edges of brain wounds. Most then continue to mature, eventually becoming oligodendrocytes capable of producing new myelin.

But Ries and Deussing also uncovered something that had not been known before. Near the damaged tissue, about one third of the OPCs activate corticotropin-releasing hormone (CRH), a hormone that plays a central role in regulating the body’s stress response. Researchers had not previously known that OPCs could produce neuropeptides such as CRH. The findings have now been published in the renowned journal Cell Reports.

The CRH response begins remarkably quickly. Production can be detected within just a few hours after an injury, but it shuts down again after roughly three days. This short and rapid burst suggests that CRH has an important function during the earliest stages of the healing response.

CRH Helps Control the Timing of Myelin Repair

One of the two known receptors for CRH also appears to be central to this process. CRH receptor 1 is present on a different population of OPCs and allows those cells to respond to the CRH that has been released.

When CRHR1 is absent, OPCs multiply more rapidly after an injury. That initial increase, however, does not translate into better repair. Ultimately, fewer mature oligodendrocytes are produced and remain.

The findings indicate that CRH helps regulate the timing of OPC maturation. That timing appears to be essential for producing enough mature oligodendrocytes to properly restore the damaged myelin sheath.

The Same System Shapes the Developing Brain

OPCs are not only important after injury. They also have a major role in building myelin as the brain matures. Much of this myelination takes place after birth and continues until young adulthood.

Because CRH receptor 1 is found on OPCs even when no injury is present, Ries and Deussing began to wonder whether the receptor might also influence myelination during normal brain development. Working with other researchers, they examined myelin formation in additional mouse models using several different methods.

They found that mice lacking CRH receptor 1 produced more OPCs during the early stages of development. Those changes did not disappear with age. Instead, they had lasting effects on the structure of the brain.

In adult brains, the researchers detected changes in myelination that could be traced to thicker myelin sheaths, particularly around thin axons. The results suggest that CRH receptor 1 on OPCs plays an important role not only in repairing myelin after injury, but also in regulating how myelin develops in the first place.

Where Does CRH Come From During Development?

Following an injury, OPCs themselves respond by producing and releasing CRH. Brain development raises a different question: where does the stress hormone come from when the brain is maturing normally?

The scientists propose that neurons may provide the answer. Their hypothesis is that developing neurons release CRH, which then influences both the multiplication of OPCs and their maturation into oligodendrocytes that produce myelin.

A Possible Connection to Depression and Stress

Neurons are already known to release CRH, particularly during stressful conditions. Stress experienced during early childhood development is also recognized as a risk factor for psychiatric disorders.

The new results therefore raise the possibility that the CRH system operating in OPCs could have broader implications for mental health.

“Our current findings suggest that in stress-associated psychiatric disorders such as depression, the CRH system in OPCs may play a greater role than previously known,” Deussing speculates.

If future research confirms and expands on that connection, understanding how CRH signaling affects OPCs, myelin formation, and brain development could eventually point toward completely new therapeutic approaches.

More than 99 percent of the upper atmosphere consists of electrically neutral gas known as the thermosphere. The term thermospheric density refers to the density of this neutral atmosphere between about 100 and 1000 kilometers above Earth’s surface. By comparison, the ionized gas of the ionosphere accounts for less than 1 percent of the atmosphere. Because ionized gas affects the way radio waves travel, the ionosphere is relatively straightforward to observe. Measuring conditions in the thermosphere is much more difficult.

A New Way to Observe the Thermosphere

Better measurements of thermospheric density could advance research into the upper atmosphere while also providing valuable information for space engineering. Motivated by both needs, researchers at Kyoto University developed a new technique for visualizing this difficult-to-observe region.

“This is a multidisciplinary study between space science and space engineering,” says corresponding author Mamoru Yamamoto. “Reading papers from both research fields, we realized that deeper dialogue between researchers from both fields is necessary.”

The researchers used publicly available orbital information from Starlink satellites and applied tomography, a technique commonly associated with medical imaging, to Earth’s upper atmosphere. By examining atmospheric drag through the gradual decay of satellite orbits, the team estimated thermospheric density around approximately 1,200 satellites flying at an altitude of 482 kilometers.

Building a Two-Dimensional Atmospheric Map

Using those measurements, the researchers produced a two-dimensional latitude-longitude snapshot of thermospheric density at an altitude of roughly 500 kilometers. According to the team, this represents the first tomographic analysis of its kind.

The resulting density patterns also showed strong consistency with observations from the European Space Agency’s SWARM satellites, which measure changes in atmospheric density along their orbital paths.

The work expands on an earlier study by the same team. In that research, scientists estimated how thermospheric density changed over time and altitude using general orbital information called Two-Line Element, or TLE, data from Starlink satellites. The new analysis adds another dimension by examining how density varies horizontally across latitude and longitude, revealing more of the thermosphere’s geographic structure.

Making Crowded Orbits Safer

The findings could have practical benefits as the number of objects orbiting Earth continues to grow. More accurate information about atmospheric density can improve predictions of satellite motion, helping reduce the chance of collisions between satellites and between satellites and space debris.

The technique could also eventually support near-real-time measurements of atmospheric density around satellites. Such monitoring could improve space weather forecasting and contribute to safer, more dependable satellite operations in the future.

Glial cells play essential supporting and nourishing roles in the brain. One type, known as astrocytes because of their star-shaped appearance, is especially important for healthy neuron function. Astrocytes provide nerve cells with nutrients, help control blood flow, and support the overall health of brain tissue.

Scientists had long thought that once astrocytes were destroyed, the adult brain could not fully replace them. This loss can occur after brain injuries and in autoimmune diseases such as the rare neuromyelitis optica spectrum disorder, in which the body’s own antibodies attack and destroy astrocytes.

Specialized Astrocytes Rebuild Damaged Brain Tissue

A study led by co-lead authors Marina Herwerth and Matthias Wyss of the Institute of Pharmacology and Toxicology at the University of Zurich (UZH) challenges that long-standing view. The research team, headed by Bruno Weber, identified a specialized population of “regenerative” astrocytes in the brains of living mice.

These cells gather around the edges of damaged brain regions and help rebuild the lost astrocyte network. “The findings of our study reveal a previously unknown ability of the adult brain to repair itself. They point toward new ways of supporting recovery from ailments involving the loss of astrocytes,” Weber says.

New Cell Nuclei Travel Into Damaged Areas

To follow the repair process, the researchers used two-photon microscopy to observe the brains of living mice in real time for several weeks. They also tracked which genes became active in different regions of the brain. Together, these methods allowed the team to identify the astrocytes responsible for restoring injured tissue.

The regenerative cells do more than simply divide. They also carry out an unusual process in which newly created nuclei from daughter cells travel considerable distances through the astrocytes toward the damaged region. As Weber explains, “they send the newly formed nuclei of their daughter cells gliding across long distances to repopulate the damaged area of the brain and knit the astrocyte network back together.”

New Targets for Brain Regeneration

The finding that cell nuclei can move through the long extensions of adult astrocytes into injured tissue adds a new dimension to scientists’ understanding of how the brain organizes its own repair after certain types of damage.

If researchers eventually learn how to selectively activate these repair mechanisms, they may be able to promote more effective restoration of damaged brain tissue, rebuild astrocyte networks, and improve recovery from certain brain disorders.

The team also identified many genes and signaling pathways that become temporarily active while the repair process is underway. These biological signals may provide potential targets for future efforts to influence regeneration after disease or injury.

“We were able to identify numerous genes and signaling pathways that are temporarily activated during repair. They could serve as starting points in the future for influencing post-disease and -injury regeneration processes,” Weber stresses.

The research focused on keratin, a natural structural protein that can be extracted from wool. When tested in a living animal, the material supported bone regeneration and produced new tissue that more closely resembled healthy, natural bone than tissue formed using the current gold standard material.

Researchers at King’s College London tested the wool-based keratin in animal models and found that it could help direct new bone growth across damaged areas.

“We are really excited to show for the first time how a wool-based material has been successfully tested in a living animal to repair bones,” said Dr. Sherif Elsharkawy at King’s Faculty of Dentistry, Oral & Craniofacial Sciences.

Wool Offers a Sustainable Source for Bone Repair

Beyond its potential medical benefits, wool could offer an important sustainability advantage. It is a naturally derived material and is often discarded as waste by the farming industry, giving it potential as both a renewable and scalable resource.

For decades, collagen has served as the gold standard scaffold in many regenerative medical and dental applications. These scaffolds act as protective barriers during healing, keeping soft tissue from interfering with the damaged area while giving new bone space to grow.

Collagen, however, has several drawbacks. The material is relatively weak and may degrade too quickly, which can limit its usefulness when repairing bones that need to bear weight or withstand force. Extracting collagen can also be complicated and costly.

“From a research perspective this is a major milestone. It positions keratin as a potential new class of regenerative biomaterial that could challenge the long-standing reliance on collagen,” said Dr. Sherif Elsharkawy.

Testing Wool Keratin as a Bone Scaffold

To investigate whether keratin could overcome some of these limitations, the researchers created membranes from keratin extracted from wool. They chemically treated the material to produce scaffolds designed to remain stable and durable.

The membranes were first tested with human bone cells in the laboratory. The cells grew well on the material and showed clear signs associated with healthy bone formation.

Researchers then moved to animal testing. They implanted the keratin membranes into rats with skull defects that were large enough that they would not normally heal on their own. Over the following weeks, the team tracked how effectively the membranes supported new bone growth across the damaged regions.

Keratin Produced More Naturally Organized Bone

The results revealed an important difference between keratin and collagen. Collagen membranes generated a greater amount of bone overall, but the bone formed with the keratin scaffolds was more organized and structurally secure. Its fibers were also better aligned, giving the new tissue a closer resemblance to natural, healthy bone.

The keratin membranes also remained stable during the healing process and integrated smoothly with the surrounding tissue. Both characteristics are important if the material is eventually to be considered for practical medical applications.

“We’ve effectively demonstrated the technology in an animal model, which makes this much more than an early materials concept. It shows that keratin can support bone regeneration in a living biological system, bringing the technology significantly closer to use in real patients,” concludes Dr. Elsharkawy.

The Hubble Space Telescope previously observed the nebula in 2000, imaging the lion face-shaped target in visible light. Those observations highlighted its distinctive appearance, including a “mane” made up of hazy structures resembling comet tails. Webb’s high-resolution instruments now provide an even sharper look at the same object.

Webb Reveals Hidden Details in the Lion Nebula

In broad terms, the Lion Nebula looks similar in Webb’s infrared observations to the structure seen earlier by Hubble. Webb observed it with both NIRCam (Near Infrared Camera) and MIRI (Mid Infrared Instrument). Its infrared capabilities, however, bring out features that are harder to see in visible light, including dense concentrations of dust and hazy regions of ionized gas.

The gas and dust now forming the nebula have been evolving for several thousand years. Even today, those materials continue to shift and change.

At the center of this activity are the remains of a dying star. In the lion-shaped appearance of the nebula, this stellar remnant resembles a small button nose. Despite its modest appearance, the star’s radiation and energy are responsible for driving many of the complex structures surrounding it.

How a Dying Star Created the Cosmic Lion

Very massive stars can end their lives in supernova explosions, but such events are relatively uncommon. Most stars in the Universe have lower masses, including the star that created NGC 2392.

When a lower-mass star reaches the point where nuclear reactions in its core can no longer support it, the star becomes unstable and begins to pulsate. As this happens, it sheds its outer layers into space. Those expelled layers form expanding shells of gas and dust known as a planetary nebula (stars at this life stage are responsible for producing much of the Universe’s observable dust).

Radiation from the exposed stellar core pushes the discarded material outward. What remains at the center is an extremely hot stellar core called a white dwarf.

In the Lion Nebula, the oxygen-rich central star has died and left behind a white dwarf that is effectively “cooking” the nebula from within. Its intense radiation is creating a bubble of ionized gas that makes up the lion’s recognizable face.

As this bubble grows, it sweeps outward and destroys dust in its path. Astronomers are still working to understand why this swept-up gas forms such complicated arrangements of rings and shells, structures that are commonly seen in planetary nebulae.

A Glowing Mane of Dust and Gas

The lion’s mane corresponds to the inner region of a dust shell illuminated by the white dwarf at the center. Within it are structures that resemble tufts of hair or comet-like tails.

These features are actually compact clumps of dust that have managed to withstand radiation from the stellar core. By blocking some of that radiation, the dense clumps also shield material located behind them.

Webb’s observations effectively “freezes” the planetary nebula at one moment in its long evolution, but the consequences of the star’s death are continuing. Gas and dust will keep traveling away from the central stellar remnant, gradually changing the nebula’s appearance.

Astronomers estimate that the Lion Nebula will eventually disperse in approximately 10,000 years. On astronomical timescales, that is a relatively brief period.

More information

Webb is the largest and most powerful telescope ever launched into space. Under an international collaboration agreement, ESA supplied the telescope’s launch service using the Ariane 5 launch vehicle.

Working with its partners, ESA was responsible for developing and qualifying the Ariane 5 adaptations needed for the Webb mission and for procuring the launch service from Arianespace. ESA also contributed the workhorse spectrograph NIRSpec and 50% of the mid-infrared instrument MIRI, which was designed and built by a consortium of nationally funded European Institutes (The MIRI European Consortium) in partnership with JPL and the University of Arizona.

Webb is an international partnership between NASA, ESA, and the Canadian Space Agency (CSA).