Dental implants have given tens of millions of people something dentures never could: a full set of fixed and fully functioning teeth. Unfortunately, 10% to 20% of implant patients eventually experience an aggressive jawbone infection called peri-implantitis. Antibiotics usually fail to stop the infection for reasons that researchers have not understood until now.

Study uncovers a surprising culprit

A recent study in PNAS Nexus by researchers with the Rutgers School of Dental Medicine has found that bacteria corrode implants, causing them to shed microscopic titanium particles into the surrounding tissue. Those particles hijack the immune cells sent to clear the infection and lock them into a state of inflammation that destroys the jawbone they are supposed to protect.

Working with human tissue samples, cultured human immune cells and a genetically engineered mouse model, the team pinpointed a specific calcium channel in the body’s bacteria-eating macrophages that the titanium particles activate. Switching that channel off in mice prevented the disease. The result is the first credible drug target for a condition that affects up to one in five implant recipients and costs the global health system more than a billion dollars a year.

“For the first time, we show why all the antibiotic treatments that work around teeth do not work around implants,” said Georgios Kotsakis, the study’s senior author and the assistant dean for clinical research at the dental school. “Now that we know the cause, we can start developing therapeutics.”

Why implants behave differently than teeth

Peri-implantitis has long been a puzzle because it initially looks like its counterpart in natural teeth, which is called periodontitis and begins with the same oral bacteria. In patients with natural teeth, antibiotics and routine cleaning resolve the infection. In patients with implants, the same drugs against the same bacteria succeed less than half the time, while the bone underneath continues to disappear.

Most research over the past 20 years has focused on the bacteria. Members of Kotsakis’s lab took a different approach and began looking at the implants. Bacteria living on the implant surface produce acidic biofilms that slowly corrode the titanium, releasing billions of particles smaller than a red blood cell. The same shedding can occur during routine cleaning, especially with instruments that dentists typically use on natural teeth.

Inside the gum, those particles get coated with a bacterial toxin called lipopolysaccharide. To the immune system, they suddenly look like enormous, indigestible bacteria. Macrophages, a type of white blood cell that surrounds and kills microorganisms, engulf them but cannot digest metal. The cells become trapped in a hyperinflammatory state, pumping out signaling molecules including interleukin-1 beta, an inflammatory protein also implicated in rheumatoid arthritis and Alzheimer’s disease.

How titanium particles hijack immunity

That inflammation eats away at bone. Worse, the immune cells lose their ability to deal with the original infection. In the lab, macrophages exposed to titanium particles took up less than half as many bacteria as unexposed cells.

“These particles are little magnets that attract the bacterial toxin, and they hijack the immune system, preventing it from clearing bacteria,” said Kotsakis. “You have a perfect storm that defies antibiotics.”

Team members traced the cascade to a calcium channel (a specialized, pore-forming protein structure within cell membranes) called TRPC1. In mice engineered without it, the immune cells handled the same titanium-plus-bacteria challenge normally: Abscesses were dramatically smaller, inflammatory cytokines dropped, and bacterial clearance was restored.

New treatment avenues and safer cleanings

Members of Kotsakis’s group are now testing drug candidates that target the same pathway in human cells.

For people who already have implants, the most useful finding may be a quieter one. The strongest known protective factor is regular professional cleaning, but the kind of cleaning matters. Until roughly a decade ago, many dentists scraped implants with the metal scalers used on teeth, a method the Rutgers lab and others have shown can itself corrode the implant and accelerate the disease. Nonabrasive techniques are now standard.

Immunotherapies such as so-called checkpoint inhibitors activate the body’s own immune system to fight cancer cells and have revolutionized the treatment of many types of tumor. In breast cancer, however, these therapies are often only of limited effectiveness. An international research team led by the Medical University of Vienna has now identified a previously underestimated mechanism by which breast tumors evade the immune system.

The findings, published in the journal Nature Communications, also provide a new starting point for improving the effectiveness of immunotherapies in breast cancer.

Sialylation is the name given to the biochemical process that the research team led by Stefan Mereiter (Department of Obstetrics and Gynecology, MedUni Vienna) and Josef Penninger (Clinical Institute of Laboratory Medicine, MedUni Vienna) has identified as a central mechanism of immune suppression in breast cancer.

This involves a specific sugar modification on the surface of tumor cells that impairs communication between cells and the immune system.

“We were able to show that around two-thirds of all breast tumors exhibit increased sialylation. In these cases, significantly fewer T-cells—i.e., immune cells that fight cancer cells—were detectable in the tumor tissue,” reports lead author Mereiter. Analyses of patient cohorts comprising a total of 136 breast cancer cases confirmed this link.

Targeted inhibition of the mechanism

In detail, the researchers discovered that sialylation, among other things, enhances the effect in the blood of the immunomodulatory growth factor G-CSF produced by cancer cells. This leads to an increased recruitment of immunosuppressive cells into the tumor, which in turn prevents cytotoxic, i.e. cell-killing, T-cells from efficiently penetrating the tumor tissue.

At the same time, sialylation makes tumor cells less recognizable to existing T cells, thereby allowing them to evade the immune system. In preclinical research models, however, the targeted pharmacological inhibition of sialylation led to T cells spreading throughout the tumor again and being able to combat it more effectively.

“More activated cytotoxic T cells reach the tumor, while at the same time, immunosuppressive neutrophil cells decrease,” explains study leader Josef Penninger.

Breast cancer is the most common cancer in women. Immunotherapies, such as so-called checkpoint inhibitors, which are designed to activate the body’s own immune system to defend against cancer cells, are only of limited effectiveness against this type of tumor.

The current study results provide both a possible explanation and a solution for this.

“Our study shows that therapeutically blocking sialylation causes even tumor models that were previously resistant to treatment to respond to immunotherapies. Our findings therefore suggest that the targeted modulation of tumor sialylation could be a promising new approach to overcoming immune-suppressive mechanisms within the tumor and thus significantly improving the efficacy of immunotherapies in breast cancer,” said Mereiter and Penninger.

The findings are now to be further investigated in additional studies within the newly established research group led by Mereiter at the Department of Obstetrics and Gynecology at MedUni Vienna, with the aim of developing future therapies.

Evening coffee has sparked controversy for years. Some people fall asleep without difficulty, while others toss and turn for half the night. However, a growing body of research suggests the question of whether coffee makes it harder to fall asleep may be too simplistic. What appears to matter far more is what happens in the brain during sleep.

Scientists studying the effects of caffeine on sleep are increasingly turning to EEG, or electroencephalography, a method used to record the brain’s electrical activity. Thanks to EEG, it is possible to observe not only sleep duration or moments of awakening, but also the biological quality of sleep itself.

“EEG allows scientists to see not only whether a person is sleeping, but also how the brain is sleeping. Classical sleep assessment measures sleep duration and its stages, whereas quantitative EEG analysis reveals more subtle changes, such as reduced slow-wave activity, which is an important marker of sleep depth and its restorative character,” said Prof. Donata Kurpas of the Department of Nursing at Wroclaw Medical University.

Slow waves are one of the key components of deep sleep, the phase responsible for bodily regeneration, restoration of energy resources, and proper brain function.

Caffeine may cause ‘shallow’ sleep

The research published in Nutrients shows the effects of caffeine do not always manifest as shorter sleep or difficulty falling asleep. Much more often, the changes concern the quality of nighttime rest.

“Caffeine may shorten sleep or make it more difficult to fall asleep. However, even when sleep duration appears normal, it may reduce slow-wave activity and shift the EEG pattern toward a more wakeful brain,” Kurpas said.

This means the body may spend eight hours in bed, but the brain may fail to fully regenerate. People are often unaware of this.

“The subjective feeling of having slept well does not always correspond to what researchers observe in neurophysiological recordings. A person may fall asleep without major difficulty and not remember awakenings, while the brain may display fewer features of deep sleep,” she added.

Why does coffee affect everyone differently?

One of the most interesting conclusions emerging from research is the enormous individual variability in response to caffeine. Genetics, metabolic rate, age, stress levels and chronic fatigue all play a role.

For some individuals, even coffee consumed in the morning may be problematic. “It is not only about coffee consumed just before bedtime. For some people, the total amount of caffeine consumed during the day and whether the body has enough time to metabolize it before nightfall may also be important,” Kurpas said.

This is particularly important information for people engaged in intellectual work, athletes and anyone who regularly uses caffeine to improve performance and concentration.

Energy is borrowed from the body

Caffeine improves alertness and reduces the sensation of fatigue, but experts point out its effects may sometimes resemble borrowing energy at the expense of nighttime regeneration.

“If caffeine helps a person function during the day while simultaneously worsening the quality of nighttime recovery, a vicious circle may develop: greater fatigue, greater need for stimulation and poorer sleep,” Kurpas said.

For this reason, modern sleep research is increasingly moving away from simple questions about sleep duration and focusing instead on how the brain functions during nighttime rest.

“Caffeine is neither good nor bad. It is a biologically active substance whose effects depend on dose, time of day, age, lifestyle, sleep quality, stress burden and individual sensitivity,” she said.

Researchers at Cincinnati Children’s have identified a potential new way to relieve chronic pain linked to neurofibromatosis type 1 (NF1), a genetic condition best known for causing tumors to grow along nerves. The new findings suggest that pain in NF1 may begin before tumors appear and may be driven by abnormal signaling from Schwann cells, which normally support and protect nerves. The abnormal signaling produces excess glial cell line–derived neurotrophic factor (GDNF), a protein that can heighten pain signaling.

The work is published in the journal Science Signaling. Namrata G. R. Raut, Ph.D., was the first author, and Michael P. Jankowski, Ph.D., was the corresponding author.

“The work helps explain why many people with NF1 report significant pain even in areas where no tumors are present,” Jankowski says. “Importantly, we also found that blocking MAPK signaling with a MEK inhibitor lowered GDNF levels in Schwann cells and reduced pain-like responses in the mice.”

NF1 affects about one in 3,000 people and can cause a wide range of symptoms, including café-au-lait spots, learning and skeletal problems, plexiform neurofibromas and chronic pain. Although tumor-related pain in NF1 is well recognized, non-tumor pain has remained poorly understood and difficult to treat. The new study focused on that gap.

Using a mouse model in which the NF1 gene was deleted in Schwann cells, the investigators found that those cells were the main source of excess GDNF. The protein acted through a receptor called GFRα1 on pain-sensing nerve fibers, helping drive mechanical hypersensitivity.

The researchers also found that using mirdametinib, a MEK inhibitor already approved for treating some NF1-related tumors, lowered GDNF levels in Schwann cells and reduced pain-like responses in the mice. The study builds on earlier work showing that Schwann cells contribute to pain signaling in NF1 and further supports the idea that non-tumor nerve changes may play a central role in the disorder.

More study is needed to confirm that the same mechanism operates in people and that it can safely relieve NF1-related pain. If that work succeeds, co-authors say it may become possible to intervene earlier to give people with NF1 tumors less pain and improved levels of day-to-day function.

Chikungunya (“to become contorted” in the Kimakonde language, named after the characteristic joint ache) is classified as one of the neglected tropical diseases by the World Health Organization. It’s caused by a virus spread by Aedes mosquitoes. Symptoms include high fever, muscle and back pain, headache, fatigue, nausea, and skin rash.

The European Center for Disease Prevention and Control has estimated that so far in 2026, there have been approximately 33,000 symptomatic cases of chikungunya worldwide, including nine deaths, predominantly in South America. Currently, the virus isn’t endemic to Europe or North America, where cases are restricted to travelers returning from tropical or subtropical regions.

But this is likely to change by 2100, argues a team of researchers in China in a new study in Frontiers in Cellular and Infection Microbiology.

“At present, 139 countries or regions—accounting for 21.3% of the world’s land area—are risk zones for the chikungunya virus. But we show that under climate change models, the virus will further expand northward into temperate regions, especially northeastern North America, central Europe, and East Asia,” said Dr. Ye Xu, a researcher at Zhejiang Chinese Medical University in Hangzhou, China, and one of the study’s corresponding authors.

A plague of mosquitos

Until recently, chikungunya was mainly transmitted by the yellow fever mosquito Aedes aegypti, a species that thrives in human settlements in the tropics.

But when scientists studied the highly publicized 2005–2006 epidemic across Réunion, Mauritius, the Comoros, and parts of India—which made approximately 266,000 people ill and caused at least 254 deaths—they detected a new mutation (“E1-A226V”) in the virus’s DNA which made it more compatible with an alternative vector, the Asian tiger moth Aedes albopictus.

Here, Xu and colleagues modeled the niche requirements of chikungunya virus and the two mosquito vectors from tens of thousands of geo-tagged records of their presence around the globe. They projected how their current ranges might change between now and 2100, based on 16 climate scenarios developed by the IPCC.

Named, for example, “green shift,” “regional rivalry,” and “fossil-fueled development,” these scenarios outline five alternative pathways for global socio-economic development. The authors also included 16 variables in their climate models, such as wind speed, elevation, precipitation, and minimum and maximum temperature.

The scientists aimed to identify emerging high-risk regions for chikungunya, to allow public health officials sufficient time to prepare for future outbreaks.

“Our results showed that climate change affects chikungunya mainly by changing where its mosquito vectors can live. In our study, the Asian tiger mosquito was especially important, explaining more than 70% of the predicted distribution of the virus,” summarized Dr. Yang Wu from the Guangzhou Customs Technology Center, likewise a corresponding author.

“Because this mosquito can tolerate cooler conditions better than the yellow fever mosquito, warming may allow it to establish in places that used to be too cold. When suitable mosquitoes become established, the chance of local chikungunya transmission increases,” explained Dr. Wu.

The time to prepare is now

The precise expansion of the disease depended on the chosen climate scenario, but north-central Europe, northeastern North America, and eastern Asia consistently turned out to be future hotspots. The authors thus counsel that these regions should put mosquito monitoring systems and suitable public health measures into place by 2040.

“The public does not need to panic, but health systems should prepare early,” warned Dr. Xu.

“For example, public health officials can act now by tracking Aedes mosquitoes, training doctors to recognize chikungunya quickly, strengthening mosquito control, and setting up rapid-response plans before outbreaks occur. These steps are especially important in temperate regions where the disease has not been a routine public-health concern.”

Limiting further global warming and investing in basic preparedness could reduce the chance that future expansion turns into large outbreaks.

Humans continuously adapt their actions and behaviors in response to changes in their surrounding environment. Past neuroscience studies suggest that this adaptation process relies on the brain’s ability to translate abstract goals or rules into specific physical actions or behaviors, yet its neural underpinnings have not yet been clearly elucidated.

Researchers at University Medical Center Tübingen and University of Tübingen recently carried out a study aimed at better understanding how context-related mental representations in a region of the brain known as the prefrontal cortex (PFC) are transformed into movement plans, which are processed in the primary motor cortex (M1). Their findings, published in Nature Neuroscience, led to the identification of a distinct communication subspace that links the PFC and M1, through which contextual information that can inform the planning of actions is transmitted.

“Adaptive behavior relies on the ability to translate abstract rules and goals into actions suited to the current context,” wrote Neha Binish, Jonas Terlau and their colleagues in their paper. “Neural population activity in the PFC has been proposed to support such flexible computations through high-dimensional dynamics, whereas activity in the M1 is related more directly to movement execution. How contextual representations in PFC are transformed into ensuing action plans within M1 remains unknown.”

Converting abstract contextual information into action plans

As part of their study, Binish, Terlau and their colleagues recorded neural activity in the brains of 12 patients with drug-resistant epilepsy, who had electrodes implanted in their brain as part of their treatment. They particularly focused on activity in the PFC and M1, as earlier works suggested that these regions play a key role in the flexible planning of future actions or behaviors.

“Previous work suggests that low-dimensional coding subspaces might organize interareal communication, but direct evidence for such population-level communication mechanisms in humans is lacking,” wrote the authors. “We use intracranial recordings from human PFC and M1 to identify a communication subspace embedded within high-dimensional PFC activity, that selectively relays behaviorally relevant information at the single-trial level.”

The study participants were asked to complete a task that required them to detect a specific target as quickly as possible, using contextual cues as guidance. When they analyzed the brain activity recorded while the participants were completing this task, using computational and statistical tools, the researchers uncovered a simplified neural signaling pathway (i.e., a communication subspace) via which contextual information appeared to be transmitted from the PFC to the M1.

“Activity in this subspace predicts context-dependent action more strongly than either region, revealing a fundamental coding principle by which coordinated interareal population dynamics filter and relay predictive information to guide context-dependent actions,” wrote Binish, Terlau and their colleagues.

Informing future research and new tech development

The recent work by Binish, Terlau and their colleagues identifies a new communication subspace between the PFC and M1 that appears to selectively transmit behaviorally relevant contextual information that can help to plan movements. As their study only involved 12 participants, further research is needed to validate their observations.

Overall, the team’s preliminary findings appear to support the idea that the brain relies on simplified communication pathways to efficiently transfer information that can inform the planning of future behaviors. If these results are confirmed in further studies, they could potentially improve the understanding of neurological or psychiatric conditions characterized by difficulties with planning future actions, including Parkinson’s disease and schizophrenia.

In the future, the researchers’ efforts might also inform the development of new technologies, including neuro-prosthetic devices and other devices that can interface with the human brain, translating people’s intentions into specific commands. Concurrently, they could also inspire the creation of new brain-inspired algorithms that plan the actions of robots, adapting to changes in their surrounding environment.