Unlike cells in the central nervous system, sensory neurons in the nasal cavity have a remarkable ability to regenerate throughout life despite near constant exposure to the outside environment.

Viral infections such as COVID-19, exposure to toxins, or even aging itself can diminish their function or the ability of these cells to replicate, which can lead to a partial or complete loss of smell. The team of researchers devised a new, easy-to-create, three-dimensional olfactory tissue mouse model or organoid to help scientists better study how neurons are continually formed in the nose and why this process might decline in disease and aging.

Their research, published recently in Cell Reports Methods, uses this mouse model to show how two types of stem cells in the nose, called horizontal basal cells (HBCs) and globose basal cells (GBCs), communicate and support each other to develop new smell-sensing nerve tissue.

“Our research suggests that these two stem cells may be interdependent,” says Brian Lin, senior author on the study and a research assistant professor in the Department of Developmental, Molecular and Chemical Biology. “One type that we thought was largely dormant — HBCs — may actually play a crucial role in supporting the production of new neurons and the repair of damaged tissue.”

Using this model, the team identified a specific subpopulation of HBCs, marked by their production of the protein KRT5, that actively support the generation of new olfactory neurons. The researchers observed that these particular HBCs play a key role in the formation of the organoids, and they found that when these cells were selectively depleted from the organoid cultures, the generation of new neurons was significantly impaired. These results suggest that these stem cells, once thought to be dormant, are essential players in the regenerative process.

“We also looked at cells from mice of different ages and grew them in the model,” Lin says. “We found a decline in the ability of the older mice cells to generate new neurons. We think this is due to a decrease in the GBC population as we age, but we need to do more work to test this hypothesis and if so, develop ways to rejuvenate them.”

An Easy-To-Use Model

Lead author of the study, Juliana Gutschow Gameiro, a former Ph.D. student visiting GSBS, came to Tufts from the State University of Londrina, Parana, in Brazil. Lin says she was dedicated to developing a model that was easy to create in labs with limited funds and equipment.

“Because loss of smell is associated with COVID-19, as well as with Parkinson’s disease and other conditions, a much larger number of researchers from a variety of different fields have begun researching olfactory epithelial cells in the last few years,” says Lin.

“We wanted to develop an easy-to-use model so that non-stem cell biologists and those working in labs with limited resources could use it to better understand how olfactory neurons regenerate and what happens that causes that process to diminish or fail completely,” he says.

Next Step: A Human Organoid

The ultimate goal is to use this mouse-tissue model of olfactory sensory neurons as a pathway to developing a human organoid that can be used to screen drugs to treat people whose sense of smell is significantly diminished or gone.

Organoids make pre-clinical trial research quicker, less expensive, and potentially more effective than using whole animals or existing human cell cultures. Organoids have already been developed for lungs, kidneys, and other organs, but not for human olfactory tissue.

“It’s challenging to get pure olfactory tissue from humans,” Lin says. Individuals are anesthetized and a brush similar to a COVID test wand is pushed deep into the nasal cavity. Unlike in their mouse model, human respiratory stem cells and olfactory stem cells collected in this process are difficult to separate.

The research team’s next challenge is to develop a simple, inexpensive technique for separating out the human olfactory stem cells and coaxing them to grow in the lab.

The research, published May 29 in Nature Sustainability, demonstrates that Australia can fully decarbonize its domestic and energy export economies by 2060 while avoiding harm to important areas for biodiversity outcomes, safeguarding agricultural activities, and respecting Indigenous land rights.

“The amount of land required for the energy transition is massive, and the speed at which we need to be deploying renewable infrastructure is unprecedented,” said first author Andrew Pascale, research scholar in the Andlinger Center for Energy and the Environment. “At the same time, we’ve shown here that not only can it be done, but that it can and should be done while incorporating the perspectives of many different stakeholders.”

If stakeholders work collaboratively to identify the most suitable areas for development, the researchers found it would be possible to site the over 110,000 square kilometers — around 1.7 times the size of Tasmania — of renewable energy infrastructure needed by 2060 to reach net-zero in Australia while preserving lands for biodiversity and agriculture.

If stakeholders refuse to compromise on their interests, however, it would lead not only to higher energy prices but also a clean energy shortfall of almost 500 gigawatts. Such a shortfall would undermine the modeled decarbonization pathway, potentially requiring an unwanted and likely costly pivot to an alternative.

“There are legitimate tensions surrounding renewable energy development,” said co-author Chris Greig, theTheodora D. ’78 & William H. Walton III ’74 Senior Research Scientist in the Andlinger Center for Energy and the Environment. “There are values — protecting biodiversity, respecting Indigenous estate, supporting farmers — that must be respected and incorporated into planning processes alongside concerns about the climate.”

The researchers drew from their prior work on the Net Zero Australia study, a multi-year, multi-institutional collaboration that charted unique pathways for Australia to fully decarbonize and maintain its domestic and export economy — a nearly $6.2 trillion task (in 2020 U.S. dollars). During Net Zero Australia, the team consulted with stakeholder groups including the National Farmers Federation, National Native Title Council, and the Australian Conservation Foundation. In the present study, the team drew from those conversations to incorporate stakeholder values about land use into their technoeconomic model, identifying the most suitable lands for renewable energy development and those that should be excluded from consideration.

“In thinking about renewable energy planning, we’re taking into account different biodiversity goals and protections for natural capital, which is critical for when you’re trying to implement projects,” said co-author James Watson, a professor of environmental management at The University of Queensland. “This is among the first works to put biodiversity and natural capital into the same picture as energy planning in Australia, which is a much-needed step in the right direction.”

The researchers combined the modeling results and stakeholder input to propose a ‘traffic-light’ approach for siting renewable infrastructure. They identified where energy projects could be easiest to site (green), where they could be potentially sited pending further stakeholder engagement (orange), and where development would be off-limits (red).

The researchers contrasted their proposed system with the renewable energy zones that the Australian Energy Regulator uses for energy planning, noting that at least two existing renewable energy zones have over 90% overlap with biodiversity exclusion areas.

“There is a difference between modeling a net-zero pathway and planning one,” Pascale said. “What looks good from the standpoint of resource quality and proximity to existing infrastructure might not hold when you simultaneously consider biodiversity and other national commitments. If 90% of the land in a proposed renewable energy zone will trigger a response from conservation groups, then it may be time to rethink.”

Greig added that at a broader level, the research highlights the importance of flexible, robust net-zero pathways that account for land-use uncertainties. Such a methodology would require moving away from conventional, top-down modeling approaches to flexible pathways that are conscious of different and sometimes competing priorities for natural capital.

“We’ve identified a need for a government planning and approval process that integrates the diverse interests of energy development, Indigenous land rights, environmental values like biodiversity, and natural resources more broadly,” said Greig. “Those perspectives are typically siloed, which is a recipe for decisions that make unacceptable tradeoffs and compromise biodiversity alongside Indigenous and farmers’ rights.”

The researchers suggested that an immediate planning goal would be to prioritize turning possible development sites (orange) into ones acceptable to diverse stakeholders (green) as quickly as possible.

They also underscored several uncertainties, such as missing critical habitat data for many Australian species and how all species might respond to climate change, which would require greater flexibility within individual transition pathways accompanied by regular model updates. If any unexpected and extreme changes in land availability exceed the flexibility designed in the pathway, the researchers acknowledged that the model’s outcomes could change.

However, Watson said that such uncertainties should not prevent planners from using the best available data to take action on renewable energy development.

“We have to deal with the problem we are facing today, thinking about where endangered species are right now and focusing on keeping those habitats intact,” said Watson. “We can take action while acknowledging we need better data, which is far preferable to simply forgetting or ignoring biodiversity.”

“I see this paper as a wake-up call,” he added. “The take-home message is that we need a clean energy future, and that we need to plan for that future — and the large spatial footprint it will require — without defeating our other societal goals.”

Neurons communicate through a process called synaptic transmission, where one neuron releases chemical messengers called neurotransmitters from a presynaptic terminal. These molecules travel across a microscopic gap called a synaptic cleft and bind to receptors on a neighboring postsynaptic neuron, triggering a response.

Traditionally, scientists believed spontaneous transmissions (signals that occur randomly) and evoked transmissions (signals triggered by sensory input or experience) originated from one type of canonical synaptic site and relied on shared molecular machinery. Using a mouse model, the research team — led by Oliver Schlüter, associate professor of neuroscience in the Kenneth P. Dietrich School of Arts and Sciences — discovered that the brain instead uses separate synaptic transmission sites to carry out regulation of these two types of activity, each with its own developmental timeline and regulatory rules.

“We focused on the primary visual cortex, where cortical visual processing begins,” said Yue Yang, a research associate in the Department of Neuroscience and first author of the study. “We expected spontaneous and evoked transmissions to follow a similar developmental trajectory, but instead, we found that they diverged after eye opening.”

As the brain began receiving visual input, evoked transmissions continued to strengthen. In contrast, spontaneous transmissions plateaued, suggesting that the brain applies different forms of control to the two signaling modes.

To understand why, the researchers applied a chemical that activates otherwise silent receptors on the postsynaptic side. This caused spontaneous activity to increase, while evoked signals remained unchanged — strong evidence that the two types of transmission operate through functionally distinct synaptic sites.

This division likely enables the brain to maintain consistent background activity through spontaneous signaling while refining behaviorally relevant pathways through evoked activity. This dual system supports both homeostasis and Hebbian plasticity, the experience-dependent process that strengthens neural connections during learning.

“Our findings reveal a key organizational strategy in the brain,” said Yang. “By separating these two signaling modes, the brain can remain stable while still being flexible enough to adapt and learn.”

The implications could be broad. Abnormalities in synaptic signaling have been linked to conditions like autism, Alzheimer’s disease and substance use disorders. A better understanding of how these systems operate in the healthy brain may help researchers identify how they become disrupted in disease.

“Learning how the brain normally separates and regulates different types of signals brings us closer to understanding what might be going wrong in neurological and psychiatric conditions,” Yang said.

“AI offers new efficiencies and opportunities, yet its deeper integration into daily life requires careful consideration to ensure that AI tools are safe, especially for adolescents,” according to the report, entitled “Artificial Intelligence and Adolescent Well-being: An APA Health Advisory.” “We urge all stakeholders to ensure youth safety is considered relatively early in the evolution of AI. It is critical that we do not repeat the same harmful mistakes made with social media.”

The report was written by an expert advisory panel and follows on two other APA reports on social media use in adolescence and healthy video content recommendations.

The AI report notes that adolescence — which it defines as ages 10-25 — is a long development period and that age is “not a foolproof marker for maturity or psychological competence.” It is also a time of critical brain development, which argues for special safeguards aimed at younger users.

“Like social media, AI is neither inherently good nor bad,” said APA Chief of Psychology Mitch Prinstein, PhD, who spearheaded the report’s development. “But we have already seen instances where adolescents developed unhealthy and even dangerous ‘relationships’ with chatbots, for example. Some adolescents may not even know they are interacting with AI, which is why it is crucial that developers put guardrails in place now.”

The report makes a number of recommendations to make certain that adolescents can use AI safely. These include:

Ensuring there are healthy boundaries with simulated human relationships. Adolescents are less likely than adults to question the accuracy and intent of information offered by a bot, rather than a human.

Creating age-appropriate defaults in privacy settings, interaction limits and content. This will involve transparency, human oversight and support and rigorous testing, according to the report.

Encouraging uses of AI that can promote healthy development. AI can assist in brainstorming, creating, summarizing and synthesizing information — all of which can make it easier for students to understand and retain key concepts, the report notes. But it is critical for students to be aware of AI’s limitations.

Limiting access to and engagement with harmful and inaccurate content. AI developers should build in protections to prevent adolescents’ exposure to harmful content.

Protecting adolescents’ data privacy and likenesses. This includes limiting the use of adolescents’ data for targeted advertising and the sale of their data to third parties.

The report also calls for comprehensive AI literacy education, integrating it into core curricula and developing national and state guidelines for literacy education.

“Many of these changes can be made immediately, by parents, educators and adolescents themselves,” Prinstein said. “Others will require more substantial changes by developers, policymakers and other technology professionals.”

Report: https://www.apa.org/topics/artificial-intelligence-machine-learning/health-advisory-ai-adolescent-well-being

In addition to the report, further resources and guidance for parents on AI and keeping teens safe and for teens on AI literacy are available at APA.org.

The right combination of certain species can provide up to 60% more nutrients than if someone ate the same quantity of even a highly nutritious species, according to an analysis by Cornell University researchers.

“This research hopefully highlights the importance of biodiversity, not just because of a moral quandary that we’re causing a mass extinction on Earth, but also because biodiversity can lead to better outcomes for fishery sustainability,” said first author Sebastian Heilpern, a postdoctoral fellow who has done previous research related to this in the Amazon River.

In the study, Heilpern and colleagues began by identifying a list of fish species that people are known to consume. Heilpern cross-checked it with existing nutrient content data for each species. From there, researchers determined the fish species that are found in every country or territory on Earth. The biogeographic and nutrient data was then fed into a computer model.

“We can then ask, out of all these combinations of potential options of species, which ones could we select and how much of each, in a way that would provide us with sufficient nutrition to meet a person’s diet [needs] with the lowest amount of fish biomass,” Heilpern said.

The model revealed that when fisheries are more biodiverse, an optimal diet that uses the lowest quantity of fish skews towards species with traits that can give them greater resilience to anthropogenic pressures like overexploitation and climate change. Such species tend to be smaller, lower on the food chain, and can be substituted with a wider range of other small species that contain similar levels of nutrients, thereby providing people with many potential alternatives.

Smaller species, like sardines, tend to be more ecologically resilient because they grow at faster rates than larger species. Additionally, optimal species are able to tolerate wider temperature ranges, making them more resilient to climate shocks.

The investigation showed that tropical coastal countries tend to have the most biodiverse fisheries, including countries in the Coral Triangle in the Pacific Ocean, Australia, India and the Amazon. The U.S. has good biodiversity, though Americans tend to consume a select few species; only 10 species account for up to 90% of fish that Americans eat.

The study was funded by the Schmidt Sciences programs, Cornell University, the National Science Foundation, the National Institute of Food and Agriculture, the Air Force Office of Scientific Research, and the David and Lucile Packard Foundation.

The study, which analyzed blood samples provided by 330 pregnant women from the Atlanta metropolitan area, is believed to be the first to investigate how exposure to ambient fine particulate matter (PM2.5) commonly found in air pollution affects the metabolism of pregnant women and contributes to increased risks of preterm and early term births.

“The link between air pollution and premature birth has been well established, but for the first time we were able to look at the detailed pathway and specific fine particles to identify how they are reflected in the increased risk of adverse birth outcomes,” says Donghai Liang, PhD, study lead author and associate professor of environmental health at the Rollins School of Public Health. “This is important because if we can figure out the ‘why’ and ‘how’ then we can know better how to address it.”

Why This Matters

Previous research has shown pregnant women and fetuses are more vulnerable than other populations to exposure to PM2.5 — which is emitted from combustion sources such as vehicle exhaust, industrial processes, and wildfires — including increased likelihood of preterm births (less than 37 weeks of gestation), which is the leading cause of death globally among children under the age of five. Preterm birth is also linked to complications such as cerebral palsy, respiratory distress syndrome, and long-term noncommunicable disease risks, while early term births (37-39 weeks of gestation) are also associated with increased neonatal morbidity and developmental challenges. Approximately 10% of the preterm births in the world are attributable to PM2.5 exposure.

Key Findings

• This was the first study to uncover the specific pathways and molecules involved in energy and amino acid metabolism that may explain how exposure to PM2.5 contributes to preterm and early term births.
• The researchers identified two substances — cortexolone and lysoPE(20:3) — as factors in the relationship between short-term air pollution exposure and elevated risk of early births, offering a potential mechanism through which air pollution triggers premature labor.
• The study highlighted disruptions in protein digestion and absorption — which are vital to fetal development and immune function — as potential links between air pollution and early births, also offering new potential targets for prevention efforts.
• Of the 330 women who participated in the Emory study, 66 (20%) delivered preterm babies and 54 (16.4%) delivered early term babies, both of which are significantly higher than the prevalence in the general U.S. population.

What The Experts Say

“As an air pollution scientist, I do not think air pollution is going away anytime soon. Even at lower levels, we continue to see harmful health effects, but we can’t just ask people to simply move away from highly polluted areas,” Liang says. “So, from a clinical intervention standpoint, that’s why it’s critical to gain a better understanding on these pathways and molecules affected by pollution. In the future, we may be able to target some of these molecules to develop effective strategies or clinical interventions that could help reduce these adverse health effects.”

Scientists at UC San Francisco have discovered how pancreatic cancer cells thrive in the lungs or liver, environments that are as distinct to cells as the ocean and desert are to animals. The spread of cancer cells to organs like these often produces the very first symptoms of pancreatic cancer. But by that time, the pancreatic cancer has spread out of control.

The findings, published May 21 in Nature, create new opportunities to treat pancreatic cancer, which is notoriously resistant to many therapies. The study was funded in part by the National Institutes of Health (NIH), the National Science Foundation (NSF), and the American Association for Cancer Research.

In the study, researchers wanted to know what allowed cells to survive in one place instead of the other. To do this, they analyzed data from MetMap, a project at the Broad Institute, an independent research organization, to find pancreatic cancer cell lines that had a tendency to colonize either the lung or the liver. Then, they looked for genomic differences that could reveal why, or even how, these cells preferred one organ over the other.

Their analysis turned up a protein called PCSK9 that controls how cells obtain cholesterol. When PCSK9 levels are low, pancreatic cancer cells consume nearby cholesterol, which is abundant in the liver. When PCSK9 levels are high, the cancer cells produce their own cholesterol. They also make molecules that protect them from damage by oxygen, a perfect adaptation to survival in the lungs.

When the team forced pancreatic cancer cells that were destined for the liver to express PCSK9, the cells made a detour to the lungs.

“Cancers persist by adapting to live in new tissues and organs, and we found that pancreatic tumors use PCSK9 to adapt as they spread,” said Rushika Perera, PhD, the Deborah Cowan Endowed Associate Professor of Anatomy at UCSF and senior author of the paper. “It opens the door to fighting metastatic cancer growth by manipulating how cells acquire their cholesterol.

Coordinated by Neurocenter Finland, this major project by the University of Eastern Finland and the University of Oulu examined the prevalence of epilepsy in patients with FTD. The research dataset is one of the largest in the world, and the results have been published in the prestigious JAMA Neurology journal.

Epilepsy occurred years before the FTD diagnosis

Epilepsy is known to be associated with Alzheimer’s disease, for example, but data on the on the connection between FTD and epilepsy remains scarce. The newly published study fills this information gap and shows that epilepsy is considerably more common in patients with FTD than previously estimated.

The study analysed patient data from the university hospitals of Kuopio and Oulu from the period 2010-2021. Out of a total of 12,490 medical records, the study identified 245 patients with FTD and 1,326 patients with Alzheimer’s disease. In addition to examining the prevalence of epilepsy in these patients, the prevalence was also examined in healthy controls.

“Our results show that epilepsy is considerably more common among those with FTD than those with Alzheimer’s disease or in healthy controls,” says Doctoral Researcher Annemari Kilpeläinen, the first author of the research article and a medical specialist in neurology.

“It is noteworthy that epilepsy occurred in some patients with FTD already ten years before their dementia diagnosis, and it was more common in all the examined stages of the disease than previous international studies have reported.”

The prevalence of epilepsy was assessed at several time points from ten years before to five years after the dementia diagnosis. In patients with FTD, the prevalence of epilepsy increased over time, and five years after the diagnosis approximately 11% had epilepsy. In addition to epilepsy diagnoses, medications used for epilepsy were more common in patients with FTD, which strengthens the reliability of the results.

Epilepsy might be left undiagnosed

Diagnosing epilepsy in patients with FTD may be challenging as the symptoms of the disease may resemble epileptic seizures. This may lead to underdiagnosis and delays in treatment. However, untreated epilepsy can significantly worsen patients’ condition.

“Identifying epilepsy is important because its treatment can improve patients’ functional capacity and quality of life. Knowledge about the association between epilepsy and FTD raises new research questions: do these diseases share some pathophysiological mechanisms and could some FTD symptoms be caused by alterations in the specific electrical systems of the brain,” says the project’s principal investigator, Associate Professor and Director of UEF Brain Research Unit Eino Solje.

An extensive research project brings together different fields of science

The recently published study is part of an extensive project that combines exceptionally extensive real-life patient data with different kinds of unique registers. The project involves a strong cooperation between the University of Oulu and the University of Eastern Finland as well as different fields of science, including between researchers in the fields of medicine and law. Kuopio University Hospital and Oulu University Hospital are part of the international European Reference Network EpiCARE and recognised centres in the field of epilepsy treatment and research.

The study was led by a team of researchers from Queen’s University Belfast, Edith Cowan University Perth (ECU), and the Medical University of Vienna and Universitat Wien.

The findings reveal that increasing the diversity of flavonoids within your diet could help prevent the development of health conditions such as type 2 diabetes, cardiovascular disease (CVD), cancer and neurological disease.

Flavonoids are found in plant foods like tea, blueberries, strawberries, oranges, apples, grapes, and even red wine and dark chocolate.

Published in Nature Food, the study tracked over 120,000 participants aging from 40 to 70 years old for over a decade. It is the first study of its kind to suggest that there is a benefit to consuming a wide range of flavonoids beyond that of simply consuming a high quantity.

ECU Research Fellow, first author and co-lead of the study Dr Benjamin Parmenter, made the initial discovery that a flavonoid-diverse diet is good for health.

“Flavonoid intakes of around 500 mg a day was associated with a 16% lower risk of all-cause mortality, as well as a ~10% lower risk of CVD, type 2 diabetes, and respiratory disease. That’s roughly the amount of flavonoids that you would consume in two cups of tea.”

Dr Parmenter added, however, that those who consumed the widest diversity of flavonoids, had an even lower risk of these diseases, even when consuming the same total amount. For example, instead of just drinking tea, it’s better to eat a range of flavonoid-rich foods to make up your intake, because different flavonoids come from different foods.

“We have known for some time that higher intakes of dietary flavonoids, powerful bioactives naturally present in many foods and drinks, can reduce the risk of developing heart disease, type 2 diabetes, and neurological conditions like Parkinson’s,” study co-lead Professor Aedín Cassidy from the Co-Centre for Sustainable Food Systems and Institute for Global Food Security at Queen’s said.

“We also know from lab data and clinical studies that different flavonoids work in different ways, some improve blood pressure, others help with cholesterol levels and decrease inflammation. This study is significant as the results indicate that consuming a higher quantity and wider diversity has the potential to lead to a greater reduction in ill health than just a single source.”

Professor Tilman Kuhn from the Medical University of Vienna, Universitat Wien and Queen’s University Belfast was also a co-lead author, noted that the importance of diversity of flavonoid intake has never been investigated until now, making this study very significant as the findings align with popular claims that eating colourful foods are invaluable to maintain good health.

“Eating fruits and vegetables in a variety of colours, including those rich in flavonoids, means you’re more likely to get the vitamins and nutrients you need to sustain a healthier lifestyle,” he said.

The first-ever dietary guidelines for flavonoids were released recently recommending increasing the consumption of flavonoids to maintain health.

“Our study provides inaugural evidence that we may also need to advise increasing diversity of intake of these compounds for optimal benefits,” Dr Parmenter said.

“The results provide a clear public health message, suggesting that simple and achievable dietary swaps, such as drinking more tea and eating more berries and apples for example, can help increase the variety and intake of flavonoid-rich foods, and potentially improve health in the long-term,” Professor Cassidy added.