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.