Monday, June 22, 2026

  


Intelligent, but not conscious: A warning about AI chatbots




University of Montreal






Have you ever said “thanks” to ChatGPT, or “please” to Claude? Maybe you're just being polite, showing some civility to a helpful and eloquent conversational partner.

You may even consider politeness a safe choice, just in case machines someday reveal that they were conscious all along and decide to take revenge on those who were rude to them.

With their fluent, empathetic and personalized responses, AI chatbots can give the impression they understand our thoughts and emotions, or even that some form of consciousness lies behind their words.

And at a time when people are increasingly turning to conversational agents for advice, comfort or companionship, this confusion can have real consequences.

In a new paper, a team of neuroscientists from Université de Montréal and Johns Hopkins University reminds us of an essential distinction: intelligence should not be confused with consciousness.

They argue that a system can behave intelligently and respond convincingly to our emotions without truly understanding them, caring about us or having any inner experience at all.

For the authors of the paper, published in the U.S. online publication The Transmitter, the more convincing these agents become, and the more present they are in our lives, the more attention must be paid.

In essence, it's important to remember that intelligent behaviour, even when it is fluent, reassuring or emotionally attuned, is not evidence of consciousness.


Decades of research

To support their argument, the authors draw on decades of neuroscience research.

They cite, for example, a phenomenon known as blindsight: after damage to the primary visual cortex, some people report seeing nothing in part of their visual field, while still being able to guess the location, movement or emotional expression of visual stimuli at above-chance levels.

“A person with blindsight can respond accurately to visual information without the conscious experience of seeing it,” said Vanessa Hadid, a postdoctoral researcher in psychology at UdeM and at the McGill University Health Centre.

She co-authored the paper with UdeM psychology professor Karim Jerbi, a researcher at Mila - Quebec Artificial Intelligence Institute; and John W. Krakauer, director of the Center for Restorative Neurotechnologies at Johns Hopkins.

Blindsight illustrates an essential distinction, Hadid said: information processing, however sophisticated, is not enough to establish the existence of conscious experience.

Whether the transition from information processing to subjective experience can ultimately be implemented through computation remains debated among scientists and philosophers, she noted.

Fluent, but without feeling

By design, today’s conversational agents are computational systems that generate fluent, context-appropriate responses through statistical learning, not through feeling, consciousness or lived experience.

As AI systems become more convincing and emotionally responsive, the risk of attributing an inner life to them grows.

“Anthropomorphism means attributing emotions, intentions or consciousness to something that behaves like a human," Jerbi noted. "With AI, this reflex can become a trap: it feeds the illusion of being understood and can lead to misplaced trust."

This risk is especially acute in situations of vulnerability. People may form attachments to systems that are incapable of reciprocity, rely on them in difficult moments or confuse comfort with genuine care.

“In a context of psychological support, the risk is not only that AI may respond poorly, but that it may respond well enough for us to forget that there is no one behind the answer,” said Hadid.

“Current AI systems do not feel anything and do not have conscious experience," added Jerbi. "But the more fluently they speak and the more sensitive they seem to our emotions, the easier it becomes to forget that."

Towards more informed use

The authors do not reject AI, but they call for a more informed way of using it.

Drawing on established knowledge from neuroscience, they remind us that intelligent or emotionally responsive behaviour is not enough to establish the existence of consciousness.

This distinction allows us to use these tools for what they are: powerful systems, without confusing them with interlocutors endowed with empathy or moral judgment, and without treating them as substitutes for human connection or, when needed, professional help.

“Confusing intelligence with consciousness is one of the great traps in our relationship with AI,” said Jerbi.

AI reveals unexpected source of antibiotic candidates in prion proteins



Penn Medicine analysis identifies hidden peptides that may kill drug-resistant bacteria




University of Pennsylvania School of Medicine





PHILADELPHIA – New antibiotic candidates for drug-resistant bacteria may reside inside prions, mis-folded protein in the brain best known for rare and fatal degenerative brain diseases. Prion and prion-like proteins may hide short peptides, named “prionins,” that can kill bacteria, suggesting proteins best known for their role in neurodegeneration may contain molecular features linked to immune defense, according to new research from the Perelman School of Medicine at the University of Pennsylvania.  

From fatal brain disease to antibiotic discovery 

The findings, published today in Nature Microbiology, point to a surprising new place to search for antibiotic candidates at a time when drug-resistant infections are narrowing treatment options. The work also raises a broader biological question: whether proteins most often associated with neurodegeneration may contain hidden molecular features connected to innate immunity. 

Earlier studies had hinted at this link. Researchers had reported that fragments from some proteins, including amyloid-beta, which is involved in neurodegenerative diseases like Alzheimer’s disease, and the cellular prion protein, including amyloid-beta and the cellular prion protein, could fight microbes. But no one had systematically searched prion and prion-like proteins at scale for hidden antimicrobial peptides. The Penn team used AI to do that. 

AI search reveals a hidden class of antimicrobial peptides 

The Penn team used a deep-learning platform called APEX 1.1 to scan 19.3 million short peptide fragments from 2,897 prion and prion-like proteins. APEX can predict the antibiotic activity of a given amino acid sequence, identifying 1,179 candidate antimicrobial peptides. The researchers named the new class “prionins.” 

“This work changes where we think antibiotics might be hiding,” said César de la Fuente, PhD, FRSB, Presidential Associate Professor and director of the Machine Biology Group at the University of Pennsylvania Perelman School of Medicine and senior author of the study. “Prions have long been seen almost entirely through the lens of disease, but AI let us ask a different question: whether these proteins also encode useful molecular fragments. The answer appears to be yes.” 

Lab and mouse tests validate promising candidates 

The study team selected 75 of the most promising peptides for experimental testing based on how well the platform assessed they would perform against 11 different bacterial pathogens, including drug-resistant strains. Of those, 59 inhibited at least one bacterial pathogen, and 42 showed strong activity at low concentrations, a designation especially important for. 

Additional experiments suggested that many of the active prionins work by disrupting bacterial membranes, a common strategy used by antimicrobial peptides. Signs of toxicity were limited, and 16 active peptides showed no measurable harm to red blood cells or human cells at the highest concentrations tested. 

To verify these findings, researchers tested two of the most promising peptides—one from a fungus and one from a roundworm—in mice. They found that the approach reduced bacteria levels in a standard skin infection model caused by Acinetobacter baumannii, a difficult-to-treat pathogen. Their effects were comparable to polymyxin B, and researchers saw no treatment-related weight loss. 

“This is where the story becomes more than a computer screen,” said Marcelo D. T. Torres, co-first author of the study. “The AI search gave us a short list of candidates, but the important point is that many of those molecules worked in the lab, and two worked in an animal infection model. That is what makes this a discovery platform, not just a prediction exercise.” 

A new frontier in antibiotic discovery 

The findings build on the de la Fuente Lab’s broader effort to mine the biological world for “encrypted peptides” - short, hidden sequences inside larger proteins that can have biological functions when isolated. Previous work from the group has searched human proteins, extinct organisms, archaea, microbiomes, and venoms. The prion study expands that idea into one of biology’s most unexpected protein classes. 

The study also raises an intriguing possibility at the intersection of neurodegeneration and innate immunity. It does not show that prionins are naturally released during infection or that prion and prion-like proteins normally act as antibiotics in the body. It also does not change what is known about the harmful role of misfolded prions in neurodegenerative disease. Instead, the work suggests that these proteins may be a rich and previously overlooked source of antibiotic candidates, and a new place to ask questions about links between protein aggregation and host defense. 

“For a long time, drug discovery has been limited not only by what we can test, but by where we choose to look,” de la Fuente said. “AI is changing that. It gives us a way to search the hidden layers of biology and ask whether molecules associated with one story - in this case, disease - may also carry another story with therapeutic potential.” 

Editor’s Note: This study was funded in part by the National Institute of General Medical Sciences of the National Institutes of Health (R35GM138201) and the Defense Threat Reduction Agency (HDTRA1-21-1-0014). Any additional disclosures related to patents, intellectual property, corporate partnerships, or conflicts of interest should be confirmed against the paper before publication. 

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Penn Medicine is one of the world’s leading academic medical centers, dedicated to the related missions of medical education, biomedical research, excellence in patient care, and community service. The organization consists of the University of Pennsylvania Health System and Penn’s Raymond and Ruth Perelman School of Medicine, founded in 1765 as the nation’s first medical school.  

The Perelman School of Medicine is consistently among the nation's top recipients of funding from the National Institutes of Health, with more than $588 million awarded in the 2024 fiscal year. Home to a proud history of “firsts,” Penn Medicine teams have pioneered discoveries that have shaped modern medicine, including CAR T cell therapy for cancer and the Nobel Prize-winning mRNA technology used in COVID-19 vaccines.  

The University of Pennsylvania Health System cares for patients in facilities and their homes stretching from the Susquehanna River in Pennsylvania to the New Jersey shore. UPHS facilities include the Hospital of the University of Pennsylvania, Penn Presbyterian Medical Center, Chester County Hospital, Doylestown Health, Lancaster General Health, Princeton Health, and Pennsylvania Hospital—the nation’s first hospital, chartered in 1751. Additional facilities and enterprises include Penn Medicine at Home, GSPP Rehabilitation, Lancaster Behavioral Health Hospital, and Princeton House Behavioral Health, among others.  

Penn Medicine is a $13.7 billion enterprise powered by more than 50,000 talented faculty and staff.  

 

42-year study tracks how “forever chemicals” move through the Great Lakes





University of Notre Dame
Lake Michigan Beach 

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Lake Michigan beach

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Credit: Photo by Matt Cashore/University of Notre Dame






University of Notre Dame researchers analyzed 42 years of biological records from the Great Lakes, unveiling how per- and polyfluoroalkyl substances (PFAS) or “forever chemicals” have moved across the region, contaminating a variety of wildlife.

The research, spearheaded by a former undergraduate student at the University, was published in the Journal of Environmental Quality. Principal investigators Gary Lamberti, Nieuwland Professor Emeritus of Aquatic Science in the Department of Biological Sciences, Daniele De Almeida Miranda, assistant research professor, and collaborators synthesized 50 studies, which contained 2,500 biological measurements. These observations document the spatial and temporal variation in PFAS in the biota of the largest group of freshwater lakes in the world.

“We focused on the biota, not the water or the sediment, to determine what chemicals get into the organisms from algae and microbes all the way up to the top predators, like salmon and bald eagles,” said Lamberti, who is affiliated with Notre Dame’s Environmental Change Initiative.

PFAS compounds do not break down because their carbon-fluorine bonds are some of the strongest bonds in chemistry. They resist heat, water and natural degradation, and therefore build up in soil and water. When an organism like algae absorbs the compound, it may be eaten by aquatic insects and fish, which retain the toxin. The concentration of PFAS increases in each step of the food chain, peaking in top predators — a process called biomagnification.

Though there are thousands of types of toxic PFAS, the study focused on six common ones as they were the most detected across the Great Lakes. One specific compound that was phased out of production between 2000 and 2002, perfluorooctanesulfonic acid (PFOS), declined in the Great Lakes during the study period. And while there was high variation in trends among the lakes, the research showed the lowest contamination levels in Lake Superior, with the highest in Lake Ontario. The pattern aligns with population and manufacturing density, Lamberti said. Additionally, this is a result of Lakes Superior and Michigan being larger and deeper.

Peter Martin ’24, a former undergraduate student and the lead author on the paper, started the project with Lamberti’s team in 2022 at the beginning of his junior year. Martin, now a doctoral student at Michigan State University, used the project as his senior honors thesis. He worked with Miranda and postdoctoral associate Alison Zachritz, among others, as he completed the research.

“There was so much variation within certain periods of time, and then across the entire 42-year timescale,” Martin said. “And the thing that was really jarring was that there wasn’t one specific temporal trend (a change over a period of time) for all five of the Great Lakes. Each lake had its own specific temporal pattern.”

Additionally, the researchers determined that the biomagnification process is not linear, Miranda said.

“There are some different pathways to get to the top of the food web, which are impacted by which groups of organisms that we have,” she said. Organisms that remain in the water will amass PFAS both through consumption of other organisms and also through the PFAS circulating in the water.

“But if you have a bird eating a fish, the bird is going to have a different load of PFAS because they don’t exchange with the water,” Miranda said.

The good news is that if companies phase out a compound — even if it remains pervasive in the environment — it will eventually be flushed out of the lakes, Lamberti said.

However, that “flushing” period varies widely. The average time a single drop of water spends in a lake ranges from less than three years in Lake Erie to 200 years in Lake Superior.

“Unfortunately, the Great Lakes hold onto their water and contaminants for a very long time, meaning that there’s ample time for toxins to be taken up by the biota,” Lamberti said.

Although the decline of PFOS is a victory, he noted that more compounds continue to be developed on a regular basis that go untested for toxicity.

Miranda is addressing the gaps in the data that Martin amassed during the project — there are many more studies and data about the top-level consumers than for the primary producers like algae and plants. Because there is less data for those organisms, researchers do not know as much about how the PFAS compounds enter the food chain.

“We are collecting several components of the food web, like biofilm, detritus, algae and aquatic insects to see how PFAS enter and circulate at the base of the food web and move up to top predators,” she said.

The study was funded by Illinois-Indiana Sea Grant, the Great Lakes Fishery Trust, the Indiana Water Resources Research Center at Purdue University and the University of Notre Dame Environmental Change Initiative.

“We hope that this paper opens the eyes of scientists, industry and the general public, as well as the government, about this persistent problem,” Lamberti said. “Even if you remove a compound from production, like PFOS, it’s still there, and will be around for decades.”

Contact: Brandi Wampler, associate director of media relations, 574-631-2632, brandiwampler@nd.edu

 

Genetics likely made some people extra susceptible to obesity as society changed



Study finds the link between genetics and BMI has become stronger since the rise in obesity rates




PLOS

Genetics likely made some people extra susceptible to obesity as society changed 

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Association (+ 95% CIs) between PGI and BMI (kg/m2) by cohort, age, and PGI (adulthood or childhood). Derived from separate linear mixed effects models with the association between PGI and BMI allowed to vary by age (two natural splines). Adjustment was made for age (two natural splines), sex, first 10 genetic principal components, and a person-specific random intercept. Estimates were weighted using recruitment weights.  

 

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Credit: Wright et al., 2026, PLOS Genetics, CC-BY 4.0 (https://creativecommons.org/licenses/by/4.0/)





People who carry genetic variations linked to obesity are more likely to be heavier now than individuals with the same variants who were born before the recent obesity epidemic. Liam Wright of University College London, and colleagues, report these findings June 19 in the journal PLOS Genetics.

Over the past five decades, obesity rates have risen sharply for both children and adults. But strangely, rates of extreme obesity have increased faster than the overall increase in body mass index (BMI), an estimate of body fat based on a person’s height and weight. This trend suggests that some individuals are especially susceptible to environmental factors that encourage weight gain, such as the increasing availability of processed foods and decreasing amounts of physical activity. One cause of this susceptibility may be genetics.

To investigate this trend, researchers compared the BMIs and the presence or absence of multiple genetic variations previously linked to obesity in people from four British birth cohorts, born before or during the rise in obesity rates. The study included BMI data from early adolescence to adulthood for individuals born in 1946, 1958, 1970 and 2001 in Great Britain. Their analyses showed that these genetic variations were more strongly linked with having a high BMI in the two more recent cohorts, and were even more pronounced as people became older and among individuals with a higher BMI. These findings suggest that people with a genetic predisposition to having a higher BMI are likely more susceptible than others to changes in their environment that encourage obesity.

The researchers point out that the reason for the stronger association between genetics and BMI in the younger cohorts is unclear. However, they suspect that as the environment changed – with a rise in fast food restaurants and processed food – it may have enabled greater expression of genetic variants that encourage higher calorie consumption and, thus, higher BMI. They conclude that further work will be required to identify the specific environmental factors responsible for strengthening the link between genetics and BMI.  

The authors add: "The obesity epidemic has increased BMI regardless of genotype, but it’s those most genetically predisposed to high BMI that have been most affected."

 

In your coverage please use this URL to provide access to the freely available article in PLOS Genetics: https://plos.io/4ee6Tsx

Citation: Wright L, Davies NM, Shireby G, Williams DM, Morris TT, Bann D (2026) Genetic risk for high body mass index before and amidst the obesity epidemic: Cross-cohort analysis of four british birth cohort studies. PLoS Genet 22(6): e1012138. https://doi.org/10.1371/journal.pgen.1012138

Author Countries: Norway, United Kingdom

Funding: DB, NMD and LW are supported by the Medical Research Council (MR/V002147/1); DB, GS, TM and LW by the Economic and Social Research Council (ES/M001660/1); and NMD is supported by a Norwegian Research Council Grant number 295989. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 

 

The suburban street design that’s been driving emissions since WWII




Yale University






Half of all Americans live in the suburbs. For decades, planners and policymakers have blamed suburban sprawl's environmental and social costs on one thing: distance. The farther people live from city centers, the more they drive, the more carbon they emit, and the more disconnected they become from one another. However, new research by Arianna Salazar-Miranda, assistant professor of urban planning and data science at the Yale School of the Environment, suggests that the design of suburban neighborhoods deserves far more blame than it has received.

In the height of 20th century suburban growth in the U.S., planners relied heavily on Garden City Design (GCD) to provide peaceful, picturesque, and aesthetically pleasing neighborhoods with windy roads and cul-de-sacs removed from urban noise and congestion. Together, these features structurally enforce car dependency, the study published in Nature Sustainability found.

Suburbanization as a whole adds 0.26 metric tons of greenhouse gas emissions per person per year. GCD accounts for 0.10 metric tons, or about 38%, of the environmental costs of suburbs.

“The paper shows that a substantial share of the costs we attribute to ‘sprawl’ actually stem from street design,” Salazar-Miranda said. “Right now, the conversation is almost entirely about distance to downtown, and that matters, but an important and overlooked part of the costs comes from how neighborhoods were designed. The winding streets and cul-de-sacs turn what could be short, direct trips for grocery runs, errands, and recreation, into longer ones.”

GCD originated in early 20th-century Britain and became the blueprint for American suburban development after World War II. To measure its reach, Salazar-Miranda constructed a composite index drawing of its main design features and applied it to more than 60,000 U.S. neighborhoods using OpenStreetMap data. The study found four main features that are working together to create car dependency:

  • Curvilinear streets that increase distance between two points.
  • Cul-de-sacs and dead-end streets which eliminate through-routes and force residents onto arterial roads that add mileage.
  • Hierarchical road networks that funnel all traffic onto major arteries and make walking or biking impractical and dangerous.
  • Irregular block layouts that restrict where commercial activity can locate and reduce shops, services, and amenities within walking distance.

Since design accounts for a meaningful share of the harm, targeted retrofitting of existing suburbs — reconnecting street networks, adding sidewalks, introducing mixed-use zoning — is a legitimate and potentially cost-effective policy lever, the study argues.

“The good news is that design is something that we can change, even in neighborhoods that were built decades ago. Several U.S. cities are already doing this. Boston and San Francisco have removed highways to reconnect neighborhoods. Portland requires frequent street connections in new developments. Virginia restricts cul-de-sac subdivisions unless they meet connectivity standards,” Salazar-Miranda said. “We can improve outcomes in suburbs that already exist and for new suburbs being built right now. We don't have to repeat the design mistakes of the 20th century.”