This means that when a telescope captures the light from a distant galaxy, the image does not reveal where that galaxy is today. It shows the galaxy as it appeared when the light began its journey. To estimate its present distance, astronomers must use a cosmological model that accounts for how the universe has expanded over time.

The leading model used today is called LCDM. It includes dark matter (different episode) and dark energy (different episode). The strengths and limitations of LCDM are worth discussing separately (different episode), but alternative models do not significantly change the overall picture described here.

The Edge of the Observable Universe

The universe is about 13.77 billion years old, but the most distant regions we can observe are now roughly 45 billion light-years away. Space expanded during the entire time that their light was traveling toward us.

This boundary is known as the particle horizon, the cosmological horizon, or the comoving horizon, depending on how stylish you feel in the moment. It defines the outer edge of our observable bubble and marks the greatest distance we can see today.

At first, the numbers seem contradictory. How can the observable universe extend 45 billion light years when the universe is only 13.77 billion years old? The answer is that the universe can expand faster than light.

Why Faster Than Light Expansion Is Allowed

This does not violate the laws of physics. The speed of light limits how quickly objects can move through space in a local region. An observer will never see a nearby rocket ship pass by faster than light.

Cosmic expansion is different. Faraway galaxies are not necessarily speeding through space in the usual sense. Instead, the space between us and those galaxies is growing. Special relativity does not place the same restriction on how quickly large distances can increase across the universe.

Astronomers can estimate how quickly a galaxy is receding by measuring its redshift. As a galaxy moves away, its light is stretched toward redder wavelengths in the electromagnetic spectrum. Edwin Hubble used this effect to uncover evidence that the universe is expanding.

In an expanding universe, more distant galaxies generally recede more quickly because a greater amount of space lies between them and us. More space means more distance that can expand.

The point at which galaxies begin receding faster than light is called the Hubble distance. It lies about 13.77 billion light-years away.

Why We Can Still See Faster Moving Galaxies

We can observe galaxies beyond the Hubble distance because the light reaching us today was emitted long ago, when those galaxies were much closer. We may also eventually receive light from some galaxies located even farther away, provided that the light began traveling toward us when the galaxies were nearer.

However, there is an ultimate limit called the cosmological event horizon (which is ever so slightly different from the black hole event horizon). It is currently about 17 billion light years away.

Any light emitted RIGHT NOW from beyond that boundary will NEVER reach us, ever, no matter how long we wait. The expansion of space will prevent it from crossing the growing distance.

Dark Energy and the Vanishing Universe

The accelerating expansion driven by dark energy makes this separation even more extreme. The cosmological event horizon will continue to expand in the future, but it will eventually approach a maximum distance of about 60 billion light years.

Even then, observers will not be able to see everything within that distance. Light from the most remote galaxies will become stretched to such enormous wavelengths that it will effectively disappear from view.

In about 100 billion years, every galaxy beyond the Local Group of galaxies will fade from sight, forever. Future observers will live in a universe that appears far smaller and emptier than the one we can see today.

In mice, the medications reduced hedonic feeding, which means eating for enjoyment rather than because the body needs energy. The drugs appeared to do this by changing activity in a reward circuit located deep inside the brain.

This newly mapped pathway is separate from the appetite-control systems previously linked to drugs such as semaglutide. Researchers say it may also offer clues about whether GLP-1 medications could eventually be used to address other problems involving reward and craving, including substance use disorder.

Oral Alternatives to Injectable GLP-1 Drugs

The University of Virginia team studied small-molecule GLP-1 receptor agonists. These compounds differ from larger peptide medications such as semaglutide, which is used in well-known drugs including Ozempic, Wegovy, and Rybelsus.

The researchers focused on orforglipron, a Food and Drug Administration (FDA)-approved oral medication, as well as the experimental small-molecule drug danuglipron. Oral compounds of this kind can be taken as pills and may cost less to manufacture than injectable GLP-1 drugs.

“As the accessibility of these medications continues to rise and patient uptake increases, it’s crucial that we understand the neural mechanisms underlying the effects we’re seeing,” said Lorenzo Leggio, M.D., Ph.D., Clinical Director of NIH’s National Institute on Drug Abuse (NIDA).

How Semaglutide and Other GLP-1 Drugs Affect Hunger

Scientists have already studied the effects of larger peptide GLP-1 drugs, such as semaglutide, extensively. Research has shown that these medications reduce hunger-driven eating by acting on networks in the hypothalamus and hindbrain.

Much less was known about what small-molecule oral GLP-1 drugs do after they enter the brain.

To investigate, the researchers used gene-editing techniques to modify GLP-1 receptors in mice, making the receptors more similar to those found in humans.

A Surprising Signal Deep in the Brain

The team gave the mice either orforglipron or danuglipron and then examined which parts of the brain became active.

As expected, the drugs affected regions already associated with appetite regulation. However, they also activated the central amygdala, an area involved in desire and reward.

This region lies deeper in the brain than scientists had previously thought GLP-1 drugs could reach directly.

Additional experiments showed that activation of the central amygdala reduced dopamine release in important parts of the brain’s reward system while the mice were eating for pleasure.

Turning Down the Reward of Food

“We’ve known that GLP-1 drugs suppress feeding behavior driven by energy demand. Now it seems oral small-molecule GLP-1s also dial back eating for pleasure by engaging a brain reward circuit,” said co-corresponding author Ali Guler, Ph.D, a professor of biology at the University of Virginia.

The findings suggest that oral GLP-1 drugs may influence more than physical hunger. They may also weaken the pleasurable reward signals that make certain foods especially tempting.

Researchers now want to determine whether these next-generation medications can reduce cravings for substances other than food. Follow-up studies will specifically examine their possible effects on substance use disorder.

Funding and Regulatory Details

NIH supported this research through the National Institute of Neurological Disorders and Stroke (NINDS) grants R01NS111220, R01NS122834, and R01NS120702, the National Institute of General Medical Sciences (NIGMS) grant R35GM140854, the National Heart, Blood, and Lung Institute (NHLBI) grant R01HL153916, and the National Cancer Institute (NCI) grant P30CA044579.

This study was not completed as a clinical trial associated with an application and has not been assessed by FDA for product approval for stated indications.

Researchers at the University of Nottingham led the INSPIRE clinical trial, which tested inulin, a natural dietary fiber found in chicory root, Jerusalem artichokes, and other vegetables. Taking inulin each day significantly reduced pain among participants with OA.

Published in the journal Nutrients, the findings indicate that supporting gut health could provide a new way to manage a widespread and disabling condition that commonly affects older adults.

A Simpler Approach to Knee Osteoarthritis

Hundreds of millions of people worldwide live with knee OA, which is a major cause of chronic pain and disability, especially later in life. Treatment often involves pain medication, which can produce side effects, or exercise programs that some patients find difficult to continue over time.

“This study raises the exciting possibility that a simple dietary change — adding a fiber supplement to your breakfast or yogurt — could meaningfully reduce pain and improve physical function,” said Dr. Afroditi Kouraki, lead author of the study from the School of Medicine at the University of Nottingham.

How Prebiotic Fiber May Influence Pain

The gut microbiome consists of trillions of bacteria that live in the digestive system and affect many aspects of health, including the way the body experiences pain. Inulin is a prebiotic, which means it provides nourishment for beneficial gut bacteria.

When these bacteria consume inulin, they produce short-chain fatty acids (SCFAs). One of the most important is butyrate, a compound that can affect inflammation and the biological pathways involved in pain throughout the body.

Participants who received inulin had higher levels of both butyrate and glucagon-like peptide-1 (GLP-1) — a gut hormone associated with pain regulation and muscle health. Increased GLP-1 levels were also linked to better grip strength, suggesting a possible connection between gut health and muscle function that researchers believe deserves further study.

Inulin and Physiotherapy Reduced Pain

The six-week randomized controlled trial included 117 adults with knee OA. Participants were divided into four groups that received inulin alone, digital physiotherapy-supported exercise (PSE) alone, both treatments together, or a placebo.

Inulin and physiotherapy each reduced knee pain independently. However, only the inulin group experienced improved grip strength and lower pain sensitivity. These measurements can reflect how the nervous system detects and processes painful signals.

The inulin group also had a much lower dropout rate. Only 3.6% of participants taking the supplement left the study, compared with 21% of those in the physiotherapy group. The difference suggests that adding a supplement to a daily routine may be easier for many patients to maintain than following an exercise program.

Dr. Kouraki said: “Our findings suggest that targeting gut health with a prebiotic supplement is a safe, well-tolerated, and effective way to reduce pain in people with knee osteoarthritis. The very low dropout rate compared to the exercise group is also encouraging from a public health perspective — people were able to fit this supplement easily into their daily lives.”

A Possible Gut-Muscle-Pain Connection

Senior author Professor Ana Valdes from the School of Medicine added: “The link we observed between GLP-1 and grip strength is particularly intriguing and points to a broader gut-muscle-pain axis that warrants further investigation. This could have implications not just for osteoarthritis, but for understanding how gut health influences ageing and physical resilience more broadly.”

Professor Lucy Donaldson, Director of Research at Arthritis UK said: “The pain of arthritis can severely impact quality of life. Our recent lived experience survey showed that six in ten people are living in pain most or all of the time due to their arthritis.

“Researchers are starting to explore the role of the gut microbiome in our experience of pain. This exciting preliminary research highlights how diet and physiotherapy can act in different ways to have benefits for people with arthritis. We know a variety and balance of healthy foods, including fiber, and regular physical activity matter, and we’re glad to be supporting research that explores how they work to help people with arthritis.”

Researchers led by Professor Ryuichi Tatsumi of Kyushu University’s Faculty of Agriculture have identified a molecule that could protect and enhance an important signal involved in muscle repair. The results were published on July 24, 2026, in Scientific Reports.

How the Body Activates Muscle Repair

The research focuses on hepatocyte growth factor, or HGF, a protein that helps initiate the repair of skeletal muscle. Under normal conditions, HGF remains inactive within the structural network surrounding muscle fibers.

When muscle tissue is injured or exposed to mechanical stimulation, HGF is released. It then attaches to c met receptors on satellite cells, the stem cells responsible for maintaining and repairing skeletal muscle. This signal brings the cells out of their inactive state, allowing them to multiply, mature, and help rebuild damaged muscle fibers.

Aging can disrupt this repair system. Previous research from the team found that HGF can undergo a chemical modification known as nitration. During this process, a nitro group is added to two locations on the protein, Y198 and Y250. These sites are located in the same region HGF uses to connect with c met.

After nitration occurs, HGF can no longer attach effectively to the receptor. The researchers compare the damaged protein to a rusted key that no longer fits its lock. This loss of function may be one of the underlying causes of muscle wasting and reduced regeneration in older adults.

“HGF is not necessarily missing as we age,” explains Tatsumi. “Rather, it can be chemically altered after it is made. That led us to wonder whether a compound with strong antioxidant capacity might protect HGF, either by preventing nitration or by compensating for the functional loss it causes.”

Testing Sulfur Based Antioxidants

The scientists investigated two compounds with strong antioxidant properties: glutathione trisulfide (GSSSG) and lipoic acid trisulfide (LASSS). Both are trisulfides, a class of molecules containing three sulfur atoms connected in sequence.

These compounds have attracted growing interest in pharmaceutical research because of their distinctive sulfur chemistry and their ability to participate in redox reactions.

Early experiments showed that both GSSSG and LASSS reduced nitration at the Y198 and Y250 sites on HGF. However, neither compound fully restored the protein’s ability to bind to its receptor.

The researchers then increased the molar ratio of HGF to trisulfide, moving from 1:4000 to 1:8000.

LASSS Creates a Stronger HGF Signal

The higher concentration produced an unexpected result. When HGF was mixed with LASSS, its ability to bind to c met rose to more than twice that of untreated HGF. The protein also became more resistant to the loss of function caused by nitration, particularly at Y198.

This improvement was seen only with LASSS. GSSSG did not produce the same effect.

“This exceeded our expectations,” comments Tatsumi. “We knew trisulfides had diverse biological functions, but we never expected that simply mixing HGF with LASSS would produce such a striking effect.

“What this tells us is that LASSS does more than simply neutralize reactive molecules. It may interact directly with HGF and induce a subtle structural change, creating an enhanced ‘Super HGF’ form that binds c-met more strongly and resists nitration.”

The findings suggest that LASSS may directly alter the structure of HGF in a beneficial way. Rather than acting only as an antioxidant, the compound may create a more active form of the protein that connects more strongly with its receptor while resisting chemical damage.

Promising Results in a Mouse Model

To determine whether the protective effect could also occur in living tissue, the team tested LASSS in mice with muscle atrophy caused by tail suspension.

Mice treated with LASSS before the procedure had significantly lower levels of nitration than untreated mice. Once again, GSSSG did not provide measurable protection. These results indicate that the beneficial effects of LASSS are not limited to laboratory experiments involving isolated proteins.

However, additional studies involving aging animals will be required to determine whether LASSS is safe and effective in vivo.

A Possible Strategy for Preserving Muscle

The discovery could support the development of new approaches for maintaining muscle repair during aging, extended bed rest, and other conditions that involve long periods of inactivity.

The researchers believe the effects of LASSS on HGF may apply across multiple species, including humans and companion animals such as cats and dogs. In the future, the approach could potentially help people maintain strength, independence, quality of life, and a longer healthy lifespan as they grow older.

The findings, published in Nature Microbiology, come from scientists at the Center for Translational Antiviral Research (CTAR). Their work focused on canine distemper virus, which produces a disease in ferrets that closely resembles measles.

Antiviral Blocks Two Routes of Transmission

The researchers tested a recently developed drug candidate called GHP-88310 (described in Science Advances). The medication is a broad-spectrum inhibitor of the viral polymerase, an enzyme the virus needs in order to reproduce.

The team examined whether prophylactic (shortly before or after exposure) use of the drug could prevent transmission through direct contact or shared air. GHP-88310 successfully blocked both forms of spread. When the drug was used to treat animals that were already infected, it also reduced the length of time they remained capable of transmitting the virus.

“Silencing measles outbreaks quickly is essential to reestablish control over the virus,” said senior author Richard Plemper, a Regents’ Professor and director of the CTAR. “This study follows our recent development of the drug candidate GHP-88310. It demonstrates that the drug is suitable to augment traditional ring vaccination against measles.”

Measles Outbreaks Return Across North America

Measles has reemerged in the United States since 2025, causing thousands of infections across several states, hundreds of hospitalizations and three confirmed deaths. Canada and Mexico have also experienced major outbreaks involving multiple deaths, raising concerns about whether North America can maintain its measles elimination status.

“We were very excited to see that GHP-88310 given by mouth completely prevented airborne transmission in our ferret model of measles,” said first author Carolin Lieber, a senior postdoctoral fellow in the Plemper lab. “This finding is unprecedented for a viral polymerase inhibitor and demonstrates the extraordinary antiviral potency of this drug.”

Tests Mimicked Homes and Classrooms

To model realistic transmission conditions, the researchers created a controlled system in which infected and uninfected animals either came into direct physical contact or shared the same airspace without touching.

“We designed the study to recapitulate viral spread between people with direct contact, for instance in a household, and between more distant social contacts, for example in classrooms or other indoor settings that bring people into proximity without direct interaction,” said Plemper. “In addition to this prophylactic benefit, GHP-88310 used therapeutically shortened the duration of disease in our model. If equally applicable to human hosts, it may shorten the severe social and economic burden of prolonged quarantine of patients and further aid outbreak management.”

Drug Candidate Moves Toward Clinical Testing

The researchers are now preparing GHP-88310 for formal clinical trials.

Other contributors to the study included Josef Wolf, Claire Ruckel and Lauren Harrison of the Center for Translational Antiviral Research in the Institute for Biomedical Sciences at Georgia State.

The research was supported by the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH).

A new study from the Buck Institute for Research on Aging, published in Aging Cell, suggests that APOE2 helps neurons protect their DNA and avoid senescence. Senescence is a damaged, poorly functioning cellular state that becomes more common with age and is believed to contribute to neurodegeneration.

The results point to a role for APOE that goes beyond its familiar involvement in cholesterol transport. They suggest that different versions of the gene may also influence how well brain cells preserve and repair their genetic material over time.

“We’ve known for years that APOE2 carriers tend to live longer and have a lower risk of Alzheimer’s, but the protective mechanism has been a black box,” says senior author Lisa M. Ellerby, PhD, professor at the Buck Institute. “Our work shows that APOE2 neurons are better at preventing and repairing DNA damage, and they resist the cellular aging program that drives so much of late-life decline. Our findings point to entirely new therapeutic directions.”

Comparing the Three APOE Variants

APOE exists in three common forms, APOE2, APOE3, and APOE4. These versions differ by only two amino acids, yet they are associated with very different effects on brain aging.

APOE4 is the strongest known genetic risk factor for late-onset Alzheimer’s disease (typically after age 65). APOE2, by contrast, has repeatedly been linked in population studies to longer life and a reduced risk of dementia.

To study how the APOE variants influence neuronal aging, the researchers used human induced pluripotent stem cells (iPSCs) that had been genetically engineered so that they differed only at the APOE locus.

The team turned these cells into two types of neurons. One group consisted of inhibitory GABAergic neurons, while the other consisted of excitatory glutamatergic neurons. The researchers then compared how APOE2, APOE3, and APOE4 affected each cell type.

They also studied hippocampal tissue from older mice engineered to carry the human APOE2, APOE3, or APOE4 gene.

APOE2 Neurons Show Less DNA Damage

The researchers found that APOE2 neurons accumulated less damage to their DNA.

Bulk and single-cell RNA sequencing showed that APOE2 GABAergic neurons strongly activated pathways involved in DNA repair and damage response. APOE4 neurons, meanwhile, displayed patterns of gene activity associated with Alzheimer’s disease.

Direct measurements of DNA strand breaks supported those findings. APOE2 neurons had significantly less DNA damage than neurons carrying the other gene variants.

Brain Cells Resist Cellular Senescence

APOE2 neurons also appeared to be more resistant to senescence.

The team exposed excitatory neurons to radiation or the chemotherapy drug doxorubicin, both of which can damage DNA and place cells under severe stress. APOE2 neurons showed lower levels of senescence markers (including p16 and CRYAB) than APOE3 and APOE4 neurons.

They also had smaller nucleoli and better-preserved nuclear architecture, both signs that the cells were maintaining a healthier internal structure.

APOE2 Protein May Transfer Some Protection

The researchers also tested whether APOE2’s protective effect could benefit neurons that carried APOE4.

When they added recombinant APOE2 protein to APOE4 neurons, the cells showed reduced DNA damage signaling after radiation exposure. The result offers an early indication that at least part of APOE2’s protective effect may be transferable rather than being limited to people born with the gene variant.

Similar Signs Appear in Mouse Brains

The mouse experiments produced a similar pattern.

Older APOE2 knock-in mice had smaller nucleoli, higher levels of the nuclear scaffolding protein Lamin A/C, and better-preserved heterochromatin in the hippocampus than mice carrying APOE3 or APOE4.

These characteristics are associated with healthier aging in brain cells and added further support to the findings from the human neuron experiments.

A New View of APOE and Brain Aging

DNA damage and cellular senescence are increasingly recognized as major contributors to aging and age-related diseases, including Alzheimer’s disease.

“Until now, the APOE field has focused largely on lipid handling and amyloid-beta biology,” says Ellerby. “By showing that APOE alleles also tune how neurons defend their genome, this study connects a major longevity gene to two of the most actively studied hallmarks of aging.”

According to Ellerby, the findings raise the possibility that treatments designed to improve DNA repair or remove senescent cells from the brain could reproduce some of APOE2’s natural benefits. Such strategies might eventually help people who carry the higher-risk APOE4 variant.

“What surprised us was how consistent the picture was across two very different neuron types and across human cells and mouse brain tissue,” said co-first author Cristian Gerónimo-Olvera, PhD, a postdoctoral fellow at the Buck Institute. “APOE2 neurons aren’t just less damaged at baseline, they recover faster when stressed.”

Future Treatments Inspired by APOE2

The researchers say they still do not know exactly how APOE2 stabilizes the nuclear envelope and strengthens DNA repair.

Future work will investigate whether APOE2-mimetic compounds or targeted DNA repair treatments can provide similar protection in people with APOE4, the group with the highest genetic risk for Alzheimer’s disease.

Other collaborators include: Stephen M. Scheeler, Carlos Galicia Aguirre, Genesis Vega-Hormazabal, Daniela Garcia, Long Wu, Natalia Murad, Kevin Schneide, Kenneth A. Wilson, Nikola T. Markov, | Jesse Simons, Akos A. Gerencser, Emily Parlan, Eric Verdin, Judith Campisi, Tara E. Tracy, David Furman, Simon Melov, Buck Institute; Sicheng Song and Sean D. Mooney, Department of Biomedical Informatics and Medical Education, University of Washington, Seattle, Washington

This work was supported by the National Institute on Aging (R01AG061879, P01AG066591, T32 AG000266), the Paul F. Glenn Center for Biology of Aging, the Hevolution Foundation (HF-PART-23-1422047), and a CatalystX award from Alex and Bob Griswold and the Valley Foundation Fellowship.