Humans are not the only primates that laugh. Chimpanzees, bonobos, gorillas, and orangutans all produce laughter, but scientists have long wondered how those vocalizations changed over millions of years and whether they could reveal anything about the origins of human language.

To investigate, researchers analyzed laughter recordings from four orangutans, two gorillas, three bonobos, four chimpanzees, and four humans. Their study, published in Communications Biology, examined 140 separate laughter sequences.

Despite the differences between species, the team found a striking similarity. Every species produced laughter with evenly spaced rhythmic intervals between successive sounds.

The researchers believe this shared rhythmic pattern originated in a common ancestor that lived around 15 million years ago. They propose that the basic structure has remained remarkably stable throughout the evolution of all living great apes.

Dr. Chiara De Gregorio, Honorary Research Associate, Department of Psychology, University of Warwick said: “How did humans evolve the remarkable ability to speak? Speech leaves no fossils, and complex language exists only in our own species. But we’ve found a 15-million-year-old clue in an unexpected place: our laughter. Unlike speech, laughter is shared by all living great apes. By comparing how different species laugh, we can see that a basic rhythmic structure has remained unchanged since our last common ancestor. That’s extraordinary.”

Human Laughter Became More Flexible

Although the underlying rhythm appears to have stayed the same, human laughter has become faster, more varied, and far more adaptable than that of other great apes.

People can consciously adjust when and how they laugh depending on the situation. A spontaneous laugh triggered by tickling differs from a polite laugh during a meeting, a nervous laugh after making a mistake, or contagious laughter shared among friends. While each serves a different social purpose, they all retain the same basic rhythmic foundation.

According to the researchers, this growing ability to control vocal timing likely developed gradually over the course of great ape evolution. That increasing level of vocal control, including over laughter, may have provided one of the essential building blocks that eventually made human speech possible.

A Window Into the Evolution of Speech

Because spoken language leaves no direct fossil evidence, scientists have few ways to trace its earliest origins. Laughter, however, is evolutionarily much older than speech and remains common to every living great ape, making it a rare opportunity to study how vocal communication evolved.

Dr. Adriano Lameria, Associate Professor, ApeTank, Department of Psychology, University of Warwick said: “It is impossible to assess the precursor forms of language directly from our extinct ancestors. Laughter, being evolutionarily older and having remained shared between all living great apes, provides a rare evolutionary window into the vocal transformations that unfolded across hominid evolution until the first humans appeared on scene. Contrary to the classic notion that the first humans suddenly acquired vocal control capacities remarkably different from their predecessors, laughter evolution tells us that humans lay on a continuum, a prolongation of vocal control capacities that were already being cumulatively honed in for 15 million years.”

The research, led by Haruka Nagaya of Hirosaki University in Japan, was published on June 10, 2026, in the open access journal PLOS One.

Vitamin C and Brain Structure

Earlier studies have suggested that people who consume more vitamin C are less likely to experience cognitive impairment as they get older. However, relatively little research has examined whether vitamin C levels measured directly in the blood are associated with physical changes in the brain.

To investigate that question, the researchers analyzed magnetic resonance imaging (MRI) scans and blood plasma samples from 2,044 Japanese adults over the age of 64.

Using the MRI scans, they measured the volume of gray matter and white matter in each participant’s brain while accounting for differences in overall brain size. They also examined connectivity within the default mode network, a group of interconnected brain regions that plays an important role in attention, autobiographical memory, and other cognitive functions.

Lower Vitamin C Linked to Smaller Gray Matter

After adjusting for factors that can also influence brain health, including age, education level, and physical activity, the researchers found a consistent pattern. Participants with lower plasma vitamin C levels tended to have reduced gray matter volume and weaker connectivity within the default mode network.

The results suggest that maintaining healthy vitamin C levels could potentially help support cognitive function and healthy brain aging. However, the researchers emphasize that this was an observational study, meaning it cannot determine whether vitamin C directly causes these differences in brain structure or function. More research will be needed to uncover the biological mechanisms behind these statistical associations.

Future studies could strengthen the evidence by measuring vitamin C levels repeatedly over time, considering additional lifestyle and dietary factors, and including participants from a wider range of ethnic and socioeconomic backgrounds.

Everyday Diet and Brain Health

Tomohiro Shintaku adds: “Our study demonstrates that higher plasma vitamin C levels are associated with better preserved structural connectivity of the default mode network (DMN), a key brain network involved in cognitive function. This finding generates the exciting hypothesis that a diet rich in vitamin C might play a supportive role in maintaining brain health and mitigating age-related cognitive decline in older adults.”

He continued: “What I found most fascinating about this research is that we were able to detect these subtle but significant associations between a single nutritional factor and large-scale brain networks by utilizing a robust, community-based cohort of over 2,000 older adults. It truly highlights the potential impact of our everyday dietary habits on our brain structures.”

Funding: The KAGOME CO., LTD. provided support in the form of salaries for authors D.K. and Y.U., but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section. Additionally, this research was supported by the Japan Agency for Medical Research and Development (AMED) under Grant Numbers JP16dk0207025 and JP21dk0207053.

Writing this week in Science, Jonathan Alder, Ph.D., and colleagues describe a combination of genetic changes that allows melanoma cells to dramatically extend their lifespan while fueling rapid tumor growth. The discovery could reshape how researchers understand melanoma and may point to new treatment strategies.

“We did something that was, in essence, obvious based on previous basic research and connected back to something that is happening in patients,” said Alder, assistant professor in the Division of Pulmonary, Allergy and Critical Care Medicine at Pitt’s School of Medicine.

Telomeres Help Control a Cell’s Lifespan

Telomeres are protective caps located at the ends of chromosomes that help keep DNA from breaking down. Every time a healthy cell divides, its telomeres become a little shorter. Eventually, they shrink to the point where the cell can no longer divide.

Keeping telomeres at the proper length is critical for health. Telomeres that become too short can cause disorders linked to premature aging and early death. On the other hand, unusually long telomeres are often associated with cancer.

Scientists have long known that melanoma tumors contain exceptionally long telomeres, especially compared with many other types of cancer.

“There’s some special link between melanoma and telomere maintenance,” said Alder. “For a melanocyte to transform into cancer, one of the biggest hurdles is to immortalize itself. Once it can do that, it’s well on its way to cancer.”

The Missing Genetic Link Behind Melanoma

The enzyme telomerase lengthens telomeres, helping protect chromosomes and preventing cells from dying. In most healthy cells, telomerase remains inactive. Many cancers, however, activate the enzyme through mutations in the telomerase gene known as TERT, allowing cancer cells to keep dividing.

Melanoma is particularly dependent on this strategy. Roughly 75% of melanoma tumors carry TERT mutations that increase telomerase production and activity.

Yet there was a mystery. Even after researchers introduced TERT mutations into melanocytes, they still could not recreate the unusually long telomeres found in melanoma tumors. That suggested another important factor was missing.

Pattra Chun-on, M.D., an internist pursuing her Ph.D. in Alder’s lab, set out to uncover that missing link. Drawing on her background in cancer biology and growing interest in telomeres, she investigated why TERT mutations alone were not enough.

“The fun part of this story is when Pattra joined my lab,” Alder said. “She contacted me and told me that she was interested in studying cancer. I told her that I study short telomeres and not long telomeres. This went on until I realized that Pattra would never take ‘no’ for an answer.”

TPP1 Completes the Puzzle

Earlier work from Alder’s laboratory had identified frequent mutations in a telomere binding protein called TPP1 while analyzing cancer mutation databases.

Chun-on discovered that these TPP1 mutations closely resembled the TERT mutations. They occurred in the newly annotated promoter region of TPP1 and boosted production of the protein. That finding immediately caught Alder’s attention because scientists had already shown that TPP1 enhances telomerase activity.

“Biochemists more than a decade before us showed that TPP1 increases the activity of telomerase in a test tube, but we never knew that this actually happened clinically,” he said.

Chun-on, who is also enrolled in a Ph.D. program in the Department of Environmental and Occupational Health at Pitt’s School of Public Health, then introduced the mutated forms of both TERT and TPP1 into cells. Working together, the two proteins produced the exceptionally long telomeres that characterize melanoma tumors.

The results revealed that TPP1 was the long sought missing factor, one that had been hidden in plain sight.

New Target for Future Melanoma Treatments

The findings offer a new explanation for how melanoma develops and survives. They also identify a cancer specific telomere maintenance system that could become a promising target for future therapies.

Additional authors of the study are Angela M. Hinchie, Agustin A. Gil Silva, Ph.D., Elizabeth Rush, Cindy Sander, Brittani K.N. Seynnaeve, M.D., M.S., John M. Kirkwood, M.D., all of Pitt, UPMC or both; Holly C. Beale, Ph.D., and Olena M. Vaske, Ph.D., both of the University of California, Santa Cruz; Carla J. Connelly, of Johns Hopkins University; and Carol W. Greider, Ph.D., of the University of California, Santa Cruz and Johns Hopkins University.

The research was supported by National Institutes of Health grants R35CA209974 and R01HL135062.

The research, led by PhD candidate Ton Sharoni and Prof. Yehu Moran at the Hebrew University of Jerusalem in collaboration with scientists from the University of North Carolina at Charlotte, was published in Nature Ecology & Evolution. It challenges the long standing idea that animals inherited a single core antiviral system from a common ancestor and instead points to multiple evolutionary solutions for resisting viral infections.

An Ancient Animal Offers New Clues About Immunity

Viruses have threatened living organisms throughout evolutionary history. In humans and other vertebrates, one of the body’s key antiviral defenses depends on a protein called MAVS. When a virus is detected, MAVS helps trigger the immune system so it can respond to the infection.

To investigate how old this defense system might be, the researchers studied sea anemones. These ancient marine animals split from the evolutionary line that eventually led to humans more than 600 million years ago. Because they are close relatives of corals and jellyfish, sea anemones provide scientists with a valuable glimpse into the early evolution of animal immunity.

During the study, the team discovered a previously unknown protein they named CARDIB (CARD Inhibitor Binding protein). At first, CARDIB looked remarkably similar to MAVS, leading researchers to believe it might perform the same antiviral role found in humans.

That assumption quickly fell apart.

“Everything about CARDIB suggested it should function like MAVS,” said Prof. Yehu Moran, head of the Department of Ecology, Evolution and Behavior at the Hebrew University. “Instead, we discovered that it does the exact opposite. Rather than activating antiviral defenses, CARDIB normally suppresses them.”

A Surprising Protein That Protects by Slowing the Immune System

The discovery immediately raised an important question. Why would an animal deliberately suppress its own immune response?

To find out, the researchers used CRISPR gene editing to remove the CARDIB gene from sea anemones before exposing them to viruses.

The results were unexpected. Sea anemones without CARDIB became much more susceptible to infection. Viruses multiplied more rapidly, the animals failed to properly activate their antiviral defenses, and their ability to fight infection dropped dramatically.

“The results were completely counterintuitive,” said Sharoni. “Although CARDIB acts as a brake on the immune system under normal conditions, that brake turns out to be essential for mounting an effective antiviral response.”

Overall, the experiments showed that sea anemones rely on an antiviral pathway that is fundamentally different from the one used by humans, even though both systems contain molecular components that look strikingly alike.

Natural Environment Confirms the Discovery

The researchers also wanted to determine whether this newly identified immune pathway mattered outside carefully controlled laboratory conditions.

To answer that question, genetically modified sea anemones were moved from laboratory aquaria into outdoor marine mesocosms supplied with natural estuarine water in South Carolina. This exposed the animals to the wide variety of viruses and microorganisms found in their normal environment.

The difference became obvious within days. Sea anemones lacking CARDIB and related antiviral genes accumulated substantially more viruses than unmodified animals. Researchers also found that one immune gene that appeared only moderately important in laboratory tests became clearly important under natural environmental conditions.

“This demonstrated that the pathway we discovered is not simply a laboratory phenomenon,” said Moran. “It plays a crucial role in helping these animals cope with the viral challenges they face in nature.”

Multiple Evolutionary Solutions to Fighting Viruses

The findings suggest that evolution did not settle on a single universal antiviral strategy. Instead, different groups of animals may have independently developed distinct molecular systems for detecting viruses and preventing them from spreading.

“Humans and sea anemones both need protection from viruses, but this work shows that evolution can organize those defenses in fundamentally different ways,” Moran added.

The research also underscores the importance of looking beyond traditional laboratory animals. Ancient organisms such as sea anemones can preserve evolutionary innovations that would remain hidden if scientists focused only on humans, mice, and other commonly studied species.

As researchers continue exploring the remarkable diversity of life, discoveries like this are revealing that evolution has repeatedly found unexpected ways to solve some of biology’s most fundamental challenges.

Now, researchers have uncovered an unexpected player in that process. In a study of mice, they found that a brain protein called Arc, which normally helps neurons communicate, also appears to help toxic Tau spread from diseased brain cells to healthy ones.

The discovery points to a possible new strategy for slowing Alzheimer’s disease. Rather than trying to eliminate Tau entirely, future treatments might stop it from reaching healthy brain cells in the first place.

“I’m excited by the fact that we’ve identified a new way of potentially stopping the progression of Alzheimer’s disease,” says Jason Shepherd, PhD, professor of neurobiology at University of Utah Health and senior author of the study.

The findings were published in the journal Cell.

How Arc Helps Toxic Tau Travel

To investigate how Alzheimer’s spreads, the researchers compared mouse models of the disease with and without the Arc protein. Their experiments showed that Arc is essential for moving toxic Tau between neurons.

Under normal conditions, Arc plays an important role in brain function. The protein packages itself inside tiny membrane bound sacs known as extracellular vesicles (EVs), which travel from one neuron to another carrying important cellular signals.

The researchers found that toxic Tau can exploit this natural communication system. By attaching itself to Arc inside these microscopic vesicles, Tau is able to travel from an unhealthy neuron into a healthy one, where it can continue spreading disease.

Tau Turns Healthy Brain Cells Toxic

Every neuron contains Tau, but in Alzheimer’s disease the protein begins clumping into large, sticky tangles that interfere with the cell’s internal transport system before eventually killing the neuron.

Mitali Tyagi, PhD, postdoctoral research associate at Washington University in St. Louis and first author of the study, who conducted the research while a neuroscience graduate student in the Shepherd Lab at U of U Health, compares these tangles to “glue monsters.”

“They glue together and block transportation within the neuron,” Tyagi explains. “But they can break down into smaller glue monsters, called Tau seeds, which can then get transferred to a new neuron. And once this Tau seed comes into contact with healthy Tau, it is able to corrupt it. So, the pathology starts all over again in a healthy neuron.”

In the Alzheimer’s mouse model, the team found extracellular vesicles containing both Arc and “sticky” Tau in brain tissue. These vesicles were capable of entering healthy cells and triggering the formation of new Tau tangles.

The picture changed dramatically when Arc was removed. Mice lacking the protein had extracellular vesicles containing very little Tau, and the disease could no longer spread effectively to neighboring brain cells.

“When we removed Arc, we saw that the transfer of Tau was severely, severely reduced,” Tyagi says. “It was almost gone.”

Arc Has Both Harmful and Helpful Effects

Although blocking Arc might sound like an obvious treatment strategy, the researchers discovered that the protein also performs an important protective role during the early stages of disease.

By helping neurons expel excess toxic Tau, Arc appears to allow damaged cells to survive longer. In mice without Arc, toxic Tau remained trapped inside neurons, causing those already sick cells to die more quickly.

“When Arc is absent, Tau becomes trapped inside neurons and accumulates to toxic levels. When Arc is present, Tau can be released in extracellular vesicles. While this helps reduce Tau buildup within the original neuron, the released Tau can be taken up by neighboring healthy neurons, promoting the spread of pathology,” Tyagi says.

These findings suggest that the most effective treatment may not be preventing diseased cells from releasing Tau. Instead, it may be better to stop those toxic extracellular vesicles from entering healthy neurons.

A Potential New Target for Alzheimer’s Therapies

The researchers also found extracellular vesicles containing both Arc and Tau in human brain tissue, suggesting the same mechanism could exist in people. However, they stress that much more research is needed before any potential therapy reaches patients.

“Most of the work we’ve been doing is in mice, not in humans,” Shepherd says. “We have some clues that whatever is happening in these mice could also be happening in humans, but we don’t know that yet. And we’re far away from saying that we’re developing a treatment for anything. But it could open new avenues to get to that point.”

One promising possibility would be to intercept Tau containing extracellular vesicles after they leave diseased neurons but before they reach healthy ones. While such an approach would not reverse existing brain damage, it could potentially slow or prevent further spread of Alzheimer’s disease.

“If we could target these particular EVs, that would be a really useful therapy strategy,” Shepherd says. “For someone with early-onset Alzheimer’s or dementia, if we could stop the spread, then we could prevent further damage and cognitive decline.”

The study, titled “Arc mediates intercellular tau transmission via extracellular vesicles,” was published in Cell.

The research was supported by the National Institutes of Health, including the Director’s Office Transformative Research Award (R01 NS115716), the National Institute of Neurological Disorders and Stroke (DSPAN F99), and the National Institute on Aging (AG073236), the Chan-Zuckerberg Initiative Ben Barres Early Acceleration Award, the Alzheimer’s Association, the McKnight Brain Disorders Award, the Jon M. Huntsman Presidential Endowed Chair fund, the Max Planck Society, AIRC IG 26229, PRIN 2022EMZJL4, the Rainwater Foundation, the JPB Foundation, and the Cure Alzheimer Fund. The Massachusetts Alzheimer’s Disease Research Center, supported by the National Institute on Aging (P30AG062421) provided human samples.

Shepherd is a co-founder of VNV, LLC and holds stock in and is a consultant for Aera Therapeutics, Inc., which licenses intellectual property and patents that include Arc capsids.