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Apple TV+ released a Season 3 trailer for its far-future sci-fi saga ‘Foundation’.

A study to look at why long-lived bats do not get cancer has broken new ground about the biological defenses that resist the disease.

Reported in the journal Nature Communications, researchers found that four common species of bats have superpowers allowing them to live up to 35 years, which is equal to about 180 human years, without cancer.

Vera Gorbunova and Andrei Seluanov, members of the University of Rochester biology department and Wilmot Cancer Institute, led the work.

Key discoveries

• Bats and humans have a gene called p53, a tumor-suppressor that can shut down cancer. (Mutations in p53, limiting its ability act properly, occur in about half of all human cancers.) A species known as the “little brown” bat—found in Rochester and upstate New York—contain two copies of p53 and have elevated p53 activity compared to humans. High levels of p53 in the body can kill cancer cells before they become harmful in a process known as apoptosis. If levels of p53 are too high, however, this is bad because it eliminates too many cells. But bats have an enhanced system that balances apoptosis effectively.
• An enzyme, telomerase, is inherently active in bats, which allows their cells to proliferate indefinitely. This is an advantage in aging because it supports tissue regeneration during aging and injury. If cells divide uncontrollably, though, the higher p53 activity in bats compensates and can remove cancerous cells that may arise.
• Bats have an extremely efficient immune system, knocking out multiple deadly pathogens. This also contributes to bats’ anti-cancer abilities by recognizing and wiping out cancer cells, Gorbunova says. As humans age, the immune system slows, and people tend to get more inflammation (in joints and other organs), but bats are good at controlling inflammation, too. This intricate system allows them to stave off viruses and age-related diseases.

How does the research apply to humans?

Cancer is a multistage process and requires many “hits” as normal cells transform into malignant cells. Thus, the longer a person or animal lives, the more likely cell mutations occur in combination with external factors (exposures to pollution and poor lifestyle habits, for instance) to promote cancer.

One surprising thing about the bat study, the researchers say, is that bats do not have a natural barrier to cancer. Their cells can transform into cancer with only two “hits”—and yet because bats possess the other robust tumor-suppressor mechanisms, described above, they survive.

Importantly, the authors say, they confirmed that increased activity of the p53 gene is a good defense against cancer by eliminating cancer or slowing its growth. Several anti-cancer drugs already target p53 activity and more are being studied.

Safely increasing the telomerase enzyme might also be a way to apply their findings to humans with cancer, Seluanov adds, but this was not part of the current study.

The National Institute on Aging supported the research.

Source: University of Rochester

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A common sleep aid restores healthier sleep patterns and protects mice from the brain damage seen in neurodegenerative disorders, such as Alzheimer’s disease, according to new research.

The drug, lemborexant, prevents the harmful buildup of an abnormal form of a protein called tau in the brain, reducing the inflammatory brain damage tau is known to cause in Alzheimer’s.

The study suggests that lemborexant and other drugs that work in the same way could help treat or prevent the damage caused by tau in multiple neurodegenerative diseases, including Alzheimer’s, progressive supranuclear palsy, corticobasal syndrome, and some frontotemporal dementias.

“We have known for a long time that sleep loss is a risk factor for Alzheimer’s disease,” says senior author David M. Holtzman, a professor of neurology at Washington University School of Medicine in St. Louis.

“In this new study, we have shown that lemborexant improves sleep and reduces abnormal tau, which appears to be a main driver of the neurological damage that we see in Alzheimer’s and several related disorders. We are hopeful this finding will lead to further studies of this sleep medication and the development of new therapeutics that may be more effective than current options either alone or in combination with other available treatments.

“The antibodies to amyloid that we now use to treat patients with early, mild Alzheimer’s dementia are helpful, but they don’t slow the disease down as much as we would like,” he adds.

“We need ways to reduce the abnormal tau buildup and its accompanying inflammation, and this type of sleep aid is worth looking at further. We are interested in whether going after both amyloid and tau with a combination of therapies could be more effective at slowing or stopping the progression of this disease.”

Holtzman and his team were among the first to identify the connection between poor sleep as a risk factor for Alzheimer’s disease and the buildup of proteins such as amyloid and tau. In past work studying mice genetically prone to amyloid and tau buildup characteristic of Alzheimer’s disease, they showed that sleep deprivation makes this buildup worse. Improving sleep in these mice with lemborexant appeared to be protective, the latest study showed, with less buildup of tau protein tangles and less nerve cell death associated with Alzheimer’s disease.

The protein tau accumulates in the brain in multiple neurological disorders, including Alzheimer’s, and causes inflammation and the death of brain cells. Holtzman and his team—co-led by first author Samira Parhizkar, an instructor in neurology—tested lemborexant in part because it has effects in parts of the brain known to be affected by abnormal tau accumulation. It also does not impair motor coordination, which is a concern for people with dementia taking hypnotic sleep aids.

Lemborexant is one of three sleep drugs approved by the Food and Drug Administration that inhibit the effect of orexins, small proteins that regulate sleep, by acting as orexin receptor antagonists. Lemborexant blocks both orexin receptors (type 1 and type 2). Receptors are proteins on the cell surface that bind to other molecules and regulate cell activity. These receptors are known to play important roles in sleep-wake cycles and appetite, among other physiological processes.

The pharmaceutical company Eisai provided lemborexant for these studies as part of a research collaboration with WashU Medicine focused on developing innovative treatments for Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative diseases.

In mice genetically prone to harmful tau buildup, lemborexant reduced brain damage compared with control mice. For example, those receiving lemborexant showed 30% to 40% larger volume in the hippocampus—a part of the brain important for forming memories—compared with control mice and those receiving a different sleep drug, zolpidem, which belongs to a different class of drugs. Zolpidem increased sleep but had none of the protective effects against tau accumulation in the brain that were seen with lemborexant, suggesting that the type of sleep aid—orexin receptor antagonist—is key in producing the neuroprotective effects. The researchers also found that the beneficial effects were only seen in male mice, which they are still working to understand.

Normal tau is important in maintaining the structure and function of neurons. When healthy, it carries a small number of chemical tags called phosphate groups. But when tau picks up too many of these chemical tags, it can clump together, leading to inflammation and nerve cell death. The authors found that by blocking orexin receptors, lemborexant prevents excess tags from being added to tau, helping tau maintain its healthy roles in the brain.

Holtzman says his team is continuing to explore the reasons lemborexant treatment’s neuroprotective effects were seen only in male mice. He speculated that the sex discrepancy could be due to the observation that female mice with the same genetic predisposition to tau accumulation developed less-severe neurodegeneration compared with male mice. With less damage to begin with, potential beneficial effects of the drug could have been smaller and more difficult to detect.

The research appears in Nature Neuroscience.

Support for this work came from the National Institutes of Health (NIH), the JPB Foundation, the Alzheimer’s Association, the Rainwater Foundation, and a COBRAS Feldman Fellowship.

Holtzman is an inventor on a patent licensed by Washington University to C2N Diagnostics on the therapeutic use of anti-tau antibodies. Holtzman cofounded and is on the scientific advisory board of C2N Diagnostics.

Source: Washington University in St. Louis

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Bed bugs are most likely the first human pest, new research shows.

Ever since a few enterprising bed bugs hopped off a bat and attached themselves to a Neanderthal walking out of a cave 60,000 years ago, bed bugs have enjoyed a thriving relationship with their human hosts.

Not so for the unadventurous bed bugs that stayed with the bats—their populations have continued to decline since the Last Glacial Maximum, also known as the ice age, which was about 20,000 years ago.

A team led by two Virginia Tech researchers recently compared the whole genome sequence of these two genetically distinct lineages of bed bugs.

Published in Biology Letters, their findings indicate the human-associated lineage followed a similar demographic pattern as humans and may well be the first true urban pest.

“We wanted to look at changes in effective population size, which is the number of breeding individuals that are contributing to the next generation, because that can tell you what’s been happening in their past,” says Lindsay Miles, lead author and postdoctoral fellow in the entomology department at Virginia Tech.

According to the researchers, the historical and evolutionary symbiotic relationship between humans and bed bugs will inform models that predict the spread of pests and diseases under urban population expansion.

By directly tying human global expansion to the emergence and evolution of urban pests like bed bugs, researchers may identify the traits that co-evolved in both humans and pests during urban expansion.

“Initially with both populations, we saw a general decline that is consistent with the Last Glacial Maximum; the bat-associated lineage never bounced back, and it is still decreasing in size,” says Miles, an affiliate with the Fralin Life Sciences Institute. “The really exciting part is that the human-associated lineage did recover and their effective population increased.”

Miles points to the early establishment of large human settlements that expanded into cities such as Mesopotamia about 12,000 years ago.

“That makes sense because modern humans moved out of caves about 60,000 years ago,” says Warren Booth, an associate professor of urban entomology. “There were bed bugs living in the caves with these humans, and when they moved out they took a subset of the population with them so there’s less genetic diversity in that human-associated lineage.”

As humans increased their population size and continued living in communities and cities expanded, the human-associated lineage of the bed bugs saw an exponential growth in their effective population size.

By using the whole genome data, the researchers now have a foundation for further study of this 245,000 year old lineage split. Since the two lineages have genetic differences yet not enough to have evolved into two distinct species, the researchers are interested in focusing on the evolutionary alterations of the human-associated lineage compared with the bat-associated lineage that have taken place more recently.

“What will be interesting is to look at what’s happening in the last 100 to 120 years,” says Booth. “Bed bugs were pretty common in the old world, but once DDT [dichloro-diphenyl-trichloroethane] was introduced for pest control, populations crashed. They were thought to have been essentially eradicated, but within five years they started reappearing and were resisting the pesticide.”

Booth, Miles, and graduate student Camille Block have already discovered a gene mutation that could contribute to that insecticide resistance in a previous study, and they are looking further into the genomic evolution of the bed bugs and relevance to the pest’s insecticide resistance.

Additional collaborators on this research are from Virginia Commonwealth University, University of Arkansas, University of Texas at Arlington, Harvard University and Broad Institute of MIT and Harvard, and the Czech University of Life Sciences.

Source: Virginia Tech

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Researchers are developing “smart” dental implants that would provide a more natural feel while chewing or talking.

Each year, millions of people in the US get dental implants as a long-term, natural-looking fix for missing teeth. But traditional implants don’t fully mimic real teeth.

Researchers recently described a new approach to dental implants that that could better replicate how natural teeth feel and function.

Their study in Scientific Reports shows early success with both a “smart” implant and a new gentler surgical technique in rodents.

“Natural teeth connect to the jawbone through soft tissue rich in nerves, which help sense pressure and texture and guide how we chew and speak. Implants lack that sensory feedback,” says Jake Jinkun Chen, a professor of periodontology and director of the Division of Oral Biology at the Tufts University School of Dental Medicine and the senior author on the study.

Traditional dental implants use a titanium post that fuses directly to the jawbone to support a ceramic crown, and the surgery often cuts or damages nearby nerves. To tie these inert pieces of metal into the body’s sensory system, the researchers developed an implant wrapped in an innovative biodegradable coating.

This coating contains stem cells and a special protein that helps them multiply and turn into nerve tissue. As the coating dissolves during the healing process, it releases the stem cells and protein, fueling the growth of new nerve tissue around the implant.

The coating also contains tiny, rubbery particles that act like memory foam. Compressed so that the implant is smaller than the missing tooth when it’s first inserted, these nanofibers gently expand once in place until the implant snugly fits the socket. This allows for a new minimally invasive procedure that preserves existing nerve endings in the tissue around the implant.

“This new implant and minimally invasive technique should help reconnect nerves, allowing the implant to ‘talk’ to the brain much like a real tooth,” explains Chen.

“This breakthrough also could transform other types of bone implants, like those used in hip replacements or fracture repair.”

Six weeks after surgery, the implants stayed firmly in place in rats, with no signs of inflammation or rejection.

“Imaging revealed a distinct space between the implant and the bone, suggesting that the implant had been integrated through soft tissue rather than the traditional fusion with the bone,” says Chen. This may restore the nerves around it.

These initial results are promising, but it will take more studies and time—for example, research in larger animal models to look at outcomes, including safety and efficacy—before trials can begin in human volunteers.

The researchers’ next step will be a preclinical study to see if brain activity confirms that the new nerves surrounding the prototype implant indeed relay sensory information.

Source: Tufts University

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Nature, Published online: 11 June 2025; doi:10.1038/d41586-025-01451-y

A quantum random-number generator has been developed that uses classical cryptography to certify that its output was produced by a quantum process.

Nature, Published online: 11 June 2025; doi:10.1038/s41586-025-09079-8

Ark+, a fully open artificial intelligence foundation model, demonstrates exceptional capabilities in diagnosing common, rare and novel thoracic diseases.

Nature, Published online: 11 June 2025; doi:10.1038/d41586-025-01779-5

Experiments in mice reveal an early postnatal window of opportunity for the effective transfer of genes to blood-cell-producing haematopoietic stem cells by injecting mice with gene-carrying lentiviral vectors. This approach showed therapeutic benefit in three mouse models of severe diseases, and could expand the applicability of haematopoietic stem-cell gene therapy in the clinic.

Nature, Published online: 11 June 2025; doi:10.1038/d41586-025-01583-1

A key component of the TCA cycle, a series of reactions that occurs in energy-generating organelles called mitochondria, can dictate the fate of intestinal stem cells.

Nature, Published online: 11 June 2025; doi:10.1038/d41586-025-01782-w

Using pulses of an ultrabright X-ray free-electron laser, the structure of liquid carbon was determined at pressures exceeding one million atmospheres and temperatures of around 7,000 kelvin. This approach revealed a complex fluid with a water-like structure and an average of four neighbouring atoms around each central carbon atom.