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<title>Biological Psychology NewsLink</title>
<link>http://www.biopsychology.com/news/</link>
<description>
Recent news articles related to the field of Biological Psychology.  
A companion to the textbook Biological Psychology by S. Marc Breedlove, Mark R. Rosenzweig, Neil V. Watson.
Published by Sinauer Associates
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<title>Brain Implant Helps a Disabled Patient Speak</title>
<link>https://www.nytimes.com/2026/09/14/well/brain-implant-helps-woman-communicate-in-real-time.html?searchResultPosition=1</link>
<description>
By Pam Belluck


In a step forward for the cutting-edge field of brain-computer interfaces, a patient with a paralyzing neurological disorder used a brain implant to converse in real time, even when she was simply thinking about what to say, a company said it would announce on Monday.

The development, by the company Paradromics, marks the latest advance for these experimental devices, known as B.C.I.s — systems that involve implanting electrodes in the brain that read neurological signals and decode those signals through artificial intelligence.

The 68-year-old Michigan woman, who has lost most of her speaking ability, was able to use the device to have spontaneous conversations via a computer-generated voice, including on the phone with her grandchildren. When she physically tried to speak, her brain generated signals that were read by the electrodes, transmitted through A.I. and displayed on the computer screen, which spoke the words aloud. The system could also produce speech when the woman imagined what to say without moving her speaking muscles.

Because the Paradromics system is wireless and doesn’t require the patient to be connected by a cord to a computer, experts said, it offers a demonstration of how patients who have lost the ability to speak might be able to eventually use the technology in their daily lives, greatly improving their ability to communicate with family, friends and co-workers.

The woman, the first patient in the Paradromics clinical trial, was implanted with the company’s Connexus B.C.I. system, which contains more than 400 electrodes, in June at University of Michigan Health.

    © 2026 The New York Times Company

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<title> Single brain implant lets paralyzed people both talk and gesture via an avatar</title>
<link>https://www.science.org/content/article/single-brain-implant-lets-paralyzed-people-both-talk-and-gesture-avatar</link>
<description>
 By Jennie Erin Smith 

The revolutionary brain-computer interfaces (BCIs) that help people with severe paralysis speak, type, move prosthetic limbs, and more are typically specialists, using sensors to pick up activity from select brain areas to perform a single function. Now, scientists have shown just one neural implant—in this case, a grid of minielectrodes surgically placed on the top part of the cortex—can do double duty, successfully “decoding” brain signals from paralyzed people as they attempt to speak as well as gesture with their upper bodies.

The technology, described today in Nature Neuroscience, can create a computer-animated image of the user in real time, which can do things such as say hello while waving, or nod while saying yes. “The authors have taken an important step toward developing highly naturalistic systems to restore function for people with paralysis,” says neurologist Daniel Rubin of Massachusetts General Hospital, whose team developed a BCI that allows users to communicate by text as quickly as able-bodied people.

The complexity of severe paralysis necessitates BCIs that can multitask, says neurosurgeon Edward Chang of the University of California (UC) San Francisco, who led the new study. People with amyotrophic lateral sclerosis (ALS) or brainstem stroke “have lost many functions,” he notes. “It’s rarely so simple that they just can’t talk or they just have a need to control a computer cursor.”

Some existing BCIs can interpret different types of signals using implants for separate functions. A group of scientists at UC Davis, for example, recently published on the successful long-term use of a BCI system relying on that strategy to help a man with ALS both speak and manipulate a cursor.

© 2026 American Association for the Advancement of Science. </description>
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<title>Map of brain ‘microproteins’ could offer new clues to Alzheimer’s disease</title>
<link>https://www.nature.com/articles/d41586-026-02914-6</link>
<description>
  Miryam Naddaf 

More than 1,000 previously overlooked ‘microproteins’ have been found in samples of human brain tissue, providing researchers with the most comprehensive database yet to study these hidden molecules inside the human brain. Dozens of the tiny proteins showed altered expression in people with Alzheimer’s disease, which could pave the way to unlocking new mechanisms of ageing and neurodegeneration.

Microproteins are small proteins with fewer than 150 amino acids and are notoriously difficult to detect with standard gene and protein sequencing techniques. In a study published in Nature Aging on 14 September1, researchers combined several methods to pinpoint the tiny molecules in postmortem samples of the dorsolateral prefrontal cortex — a region of the brain involved in cognitive control — from people with and without Alzheimer’s disease.

The team identified more than 4,300 microproteins, creating the largest atlas of microproteins in Alzheimer’s disease made so far.

“We might be actually missing a whole layer of biology by overlooking these microproteins,” says Bahareh Ajami, a neuroimunologist at Cedars-Sinai Medical Center in Los Angeles, California.

“Alzheimer’s disease is a proteinopathy [wherein] the pathology is in part due to the proteins that have misfolded or accumulated and evoked a toxic response,” says study co-author Brendan Miller, a neuroscientist at the Salk Institute for Biological Studies in San Diego, California. “It should be somewhat urgent to understand the full proteome”, including microproteins, he adds.

© 2026 Springer Nature Limited
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<title>Is There Anything a Fruit Fly Brain Can’t Do?</title>
<link>https://www.nytimes.com/2026/09/15/technology/fruit-fly-brain-map-google.html</link>
<description>
By Michael Levenson

What can a fruit fly do? Buzz around ripe bananas, sure. But maybe, a whole lot more. Like parallel park. Or play Minecraft.

Creative internet users have in recent days taken a complete map of a fruit fly’s 166,000 neurons, published by Google, and made simulated flies do some things that are pretty impressive, given that these insects have a brain the size of a poppy seed. One has been trained to solve a Rubik’s Cube. Another dances to the Village People’s “Y.M.C.A.” in response to four tones. Others have envisioned fruit flies playing poker and blackjack and slicing a doner kebab.

In general, the goal of these engineers and artists is not to show what a fly can do, but “what’s the dumbest thing we can make it do,” said Mark Unthank, a software developer who got a fly to parallel park a car after hundreds of failed attempts. Mr. Unthank, who lives in Italy, also programmed a fly to use a car’s blinkers when turning because he was frustrated that so few human drivers seem to use them.

“That’s how easy it is,” he said. “Even a fly could do it.”

Producing the map of the fly’s brain, on the other hand, was anything but easy. It was serious research meant to advance the study of neuroscience.

For years, researchers worked to develop sophisticated imaging techniques to map the connections within the nervous systems of various organisms. Some have focused on fruit flies because of the insect’s relative lack of complexity; while the fly has just 166,000 neurons, a human being has about 86 billion.

    © 2026 The New York Times Company

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<title> Infant memories: Lost but not gone?</title>
<link>https://www.thetransmitter.org/memory/infant-memories-lost-but-not-gone/</link>
<description>
By Paul Frankland, Sheena Josselyn, Nick Turk-Browne

What is your first memory? A birthday party, a fall in the playground, a family trip? For most people, it dates to around age 3 or 4 at the earliest. Infant and toddler experiences are, seemingly, absent from our autobiography. Sigmund Freud named this phenomenon infantile amnesia and argued that early-life memories are so emotionally charged that they must be actively repressed. In this view, infants are capable of forming memories for important life events, but these memories become inaccessible over time (although he argued that psychotherapy might, in principle, recover them).

More contemporary psychological accounts have linked infantile amnesia to the immaturity of the hippocampus, a brain structure critical for forming episodic memories in older children and adults. According to these accounts, hippocampal circuits are not sufficiently developed in infancy to form enduring traces of life events. That is, infantile amnesia reflects a failure to encode experiences. 

Here, we argue for a different view. Early-life experiences are encoded by the hippocampus and may persist over time. What changes is how easily they can be accessed. Infantile amnesia, therefore, reflects not a failure to encode memories but a failure to naturally retrieve them.

Infantile amnesia is not uniquely human. Nearly all mammals that have been studied exhibit accelerated forgetting in infancy. For example, similar to young children, mice and rats can form memories of specific events, but these memories do not endure. This phenomenon has been demonstrated across a range of infant-acquired experiences, including fear conditioning, object recognition and spatial learning. The exception is highly precocial animals, such as guinea pigs and degus, whose brains are much more mature at birth.
. 

© 2026 Simons Foundation
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<title>How Sleepy Dogs and Collapsing Mice Taught Scientists About Narcolepsy</title>
<link>https://www.nytimes.com/2026/09/09/science/narcolepsy-sleep-lasker-award-researchers.html</link>
<description>
By Carolyn Y. Johnson

Sleep is mysterious, and it took sleepy animals, serendipity and competition to begin to unravel its precise biology.

In the late 1990s, Dr. Masashi Yanagisawa at the University of Texas Southwestern Medical Center discovered two brain chemicals in rodents that seemed to be instrumental in stimulating hunger. He called them “orexins,” a play on “orexis” the Greek word for appetite.

At the same time, Dr. Emmanuel Mignot at Stanford University School of Medicine was hunting for the root cause of an inherited form of narcolepsy in Doberman pinschers, Labrador retrievers and Dachshunds.

In back-to-back studies published in the summer of 1999, these two lines of research unexpectedly converged, breaking open the neurobiology of sleep and identifying a root cause of the sleep disorder narcolepsy, which affects an estimated one in every 2,000 people in the United States. A new narcolepsy drug based on these insights was approved in August.

On Wednesday, Dr. Yanagisawa, now at the University of Tsukuba in Japan, shared the Albert Lasker Basic Medical Research Award with Dr. Mignot, for their work into the nature of sleep. The prestigious prizes are often called “America’s Nobel.”

“Their work has cracked open a molecular dissection of sleep regulation, reinforced the immune system’s involvement in human narcolepsy, and pointed toward new treatments for this illness and other sleep disturbances,” the Lasker citation said. The field is now a major target of pharmaceutical companies, but their basic science research was supported largely by philanthropy and federal funding.

Thirty years ago, it was far from clear that these scientists were studying the same problem.

    © 2026 The New York Times Company

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<title>New Drug Lifts the Fog of Sleepiness for Those With Narcolepsy</title>
<link>https://www.nytimes.com/2026/09/09/science/narcolepsy-drug-orzeyful-neuroscience.html</link>
<description>
By Carolyn Y. Johnson

Many people have a cartoonish idea of narcolepsy, perhaps picturing someone falling asleep standing up.

What people don’t understand is that sleepiness can infiltrate every aspect of daily life, said Julie Flygare, 42, who was diagnosed with the sleep disorder in 2007, during her second year of law school. It interferes with memory, attention and weighs down everyday existence like a “heaviness on the skull,” she said.

While taking her current medications, Ms. Flygare has four to six precious hours of wakefulness a day, and still needs a nap. Positive feelings, like, say, the joy of hitting a volley in tennis, trigger episodes of cataplexy; her muscles go slack and her grip on the racket loosens. She, like many other patients, struggled for years to be correctly diagnosed and to find the right combination of stimulants or other drugs to ease her symptoms.

Since then, Ms. Flygare has been waiting, and pushing for, a drug aimed not just at alleviating sleepiness, but at replacing a crucial missing brain chemical. Last month, she saw it happen. A first-of-its-kind drug for the sleep disorder narcolepsy was approved by the F.D.A., offering a new treatment for people who live with the debilitating fog of sleepiness.

The new drug developed by Takeda Pharmaceutical Co., called Orzeyful, marks a long-sought success in the quest to mimic an essential brain peptide called orexin, which is missing in people with type 1 narcolepsy. About 120,000 people in the United States suffer from this type of narcolepsy, which causes pervasive sleepiness and episodes of cataplexy. Other companies, including Alkermes and Eli Lilly, are chasing close behind.

To test narcolepsy treatments, doctors use a “maintenance of wakefulness test” in which a person sits in a dim room for 40 minutes.

    © 2026 The New York Times Company

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<title>Listening for schizophrenia: How AI could help with early diagnosis</title>
<link>https://knowablemagazine.org/content/article/mind/2026/how-ai-can-listen-for-signs-of-schizophrenia</link>
<description>
By Astrid Landon 

Schizophrenia is tough to diagnose. Patients may present with hallucinations (sometimes), social withdrawal (maybe) or delusions (not always). More generally, they just sound unlike themselves. Clinicians rely on their expertise and subtle cues to determine how different patients’ speech is, along with which symptoms appear over time, to justify leaning toward schizophrenia rather than another mental illness. This leads to delays in diagnosis. Americans with psychotic disorders — more than 3 million of whom have schizophrenia — receive a diagnosis a year and a half, on average, after their first symptoms appear.

Researchers are now investigating whether artificial intelligence could improve diagnosis and care by listening to and analyzing what clinicians can’t hear or quantify, even if the software is working off just a few minutes of conversation. AI won’t make its grand entrance into the clinic tomorrow. But it’s being hailed as the new frontier in psychiatric care, one that could enable early, accurate detection and personalized monitoring of illnesses based on indistinct symptoms.

“We have the tools to do that with the kind of precision that we have never had before,” says Thomas Insel, a psychiatrist and neuroscientist who led the US National Institute of Mental Health for 13 years.

Schizophrenia is a disorder that interferes with people’s perception of reality, their thinking and their emotional regulation. It affects about 23 million people worldwide and is usually diagnosed between the late teens and early 30s. No one knows what causes it, but research suggests it could be a combination of genetics, environment, brain chemistry and substance use.

Clinicians stress the importance of detecting the disorder as early as possible, because the longer it is left untreated, the poorer the response to treatment and the greater the risk of brain tissue loss, worsening symptoms and suicide. But psychiatrists often make errors.

© 2026 Annual Reviews
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<title> Finally, a new route for the magnetic-sense field</title>
<link>https://www.thetransmitter.org/sensory-systems/finally-a-new-route-for-the-magnetic-sense-field/</link>
<description>
By Calli McMurray

When newcomers join the band of biologists who study the magnetic sense of animals, they have 60 years of conflict to catch up on. 

They might be warned that it’s an “unhappy area of science,” as Eric Warrant, professor and head of sensory biology at Lund University, describes it. They might hear about the infamous incident from the 2011 Royal Institute of Navigation meeting, where a new member of the field gave a talk that unraveled a finding that had already made its way into textbooks. Or they might learn about the failed attempt to replicate a key finding in fruit flies, and how that derailed 15 years of work.

But they will almost certainly hear about the two main theories of how the magnetic sense works—one based on magnetic crystals, the other on quantum chemistry—and how the two camps have been locked in a stalemate for years.

Now, new data from migratory insects is poised to provide the direct evidence the field has long needed, and a study last year in sea turtles suggests multiple mechanisms could be at play, even in the same species. Those could be enough to break the logjam and open the field back up again.

David Keays, professor of neurobiology at Ludwig-Maximilians-Universität München, who gave the game-changing talk at the 2011 meeting, is one of the many scientists who have spent the majority of their careers wanting to know how this sense works. Finally, he says, “I think we are getting closer.” 

When the study of the magnetic sense, also called magnetoreception, first materialized, it wasn’t taken seriously enough to generate any debates at all.

© 2026 Simons Foundation
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<title>Are Too Many Americans Taking Antidepressants?</title>
<link>https://nautil.us/are-too-many-americans-taking-antidepressants-1284975</link>
<description>
By Andrew McLean

Drugs for treating depression are among the most prescribed category of medications in the U.S.—1 in 6 American adults take them.

Some health researchers and advocates have raised concerns that too many patients are using antidepressants and that patients who want to stop taking them struggle to do so. One of the most prominent voices on this point is Health and Human Services Secretary Robert F. Kennedy Jr., who launched an effort in May 2026 encouraging doctors to find other ways besides antidepressants and other psychiatric drugs to treat depression when possible.

As a psychiatrist for over 35 years, including a past role as the medical director of North Dakota’s Department of Human Services, I’ve seen both the benefits and the problems with antidepressants. In my view, there are grains of truth to claims that they are overused, but the full picture is much more nuanced.

What Are Antidepressants, and Who Takes Them?

Over half of all antidepressant medications prescribed are a type of drug called selective serotonin reuptake inhibitors, or SSRIs. The first SSRI—fluoxetine, better known by its brand name Prozac—was approved in 1987. A handful of other types of SSRIs, which work through different mechanisms, also exists.

Antidepressants can be helpful for moderate to severe depression, but they are typically not warranted for mild depression, as the side effects might outweigh any potential benefits. For mild depression, many effective nonmedication treatments exist.

However, the distinction between mild and more severe symptoms sometimes gets lost. In everyday language, people use the term “depression” to describe everything from a minor sense of the blahs to a serious clinical condition requiring treatment.
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<title>Psilocybin May Prevent Nerve Damage Caused by Chemotherapy</title>
<link>https://www.nytimes.com/2026/09/03/health/psilocybin-cancer-nerve-damage.html</link>
<description>
By Andrew Jacobs

Can psilocybin, the hallucinogenic compound also known as magic mushrooms, inoculate cancer patients against the debilitating nerve damage caused by chemotherapy? At first blush, such an outcome might seem like magical thinking.

But a study published on Thursday in the journal Science makes a compelling case that administering psilocybin shortly before cancer treatments might prevent chemotherapy-induced peripheral neuropathy, a condition that affects about two-thirds of patients who receive chemo.

The scientists studied mice, but the results are so promising that human trials are beginning this month. If successful, the treatment could revolutionize cancer therapy and improve the quality of life for millions.

There are no effective treatments for neuropathy, which causes pain, tingling and numbness in the hands and feet, and can force patients to scale back or halt chemotherapy when the discomfort becomes too much to bear.

For some cancer survivors, the condition persists for years after treatments end.

The study, by a team of doctors and researchers at the University of Texas MD Anderson Cancer Center, found that lab mice given two doses of psilocybin before receiving chemotherapy were shielded from nerve damage.

The protection held up through six consecutive chemo sessions and persisted for eight months, the study’s duration. Just as important, the psilocybin treatments, given as a pill, had no impact on tumor growth or immune response, making them safe for even the sickest patients.

    © 2026 The New York Times Company

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<title>Why are human births so difficult? Male babies—not just upright walking—may be to blame</title>
<link>https://www.science.org/content/article/why-are-human-births-so-difficult-male-babies-not-just-upright-walking-may-be-blame</link>
<description>
 By Bridget Alex 

One of the biggest downsides of upright walking in humans is the so-called obstetrical dilemma. Babies born with big brains—and thus big heads—must fit through a relatively narrow pelvis shaped for bipedal locomotion. These clashing demands, it’s been suggested, have made human births especially grueling compared with other mammals.

But recent studies have questioned the simplicity of this explanation—and whether the phenomenon is even unique to humans. Reporting this month in The Anatomical Record, researchers add another wrinkle to the obstetrical dilemma: fetal sex.

Reviewing birth data for 140 species, the authors argue sons are more difficult to birth than daughters for many mammals, including humans and our ancient ancestors. This added risk may be offset by an evolutionary reward: Bigger male babies grow into bigger male adults, who tend to have more grandbabies, meaning more of that mother’s genes are passed down.

“Natural selection doesn’t care if it’s easy. It cares if it works,” says Anna Warrener, an anthropologist at the University of Colorado Denver who was not involved with the study. Still, she says the authors may be overinterpreting their finding.

Every day, about 700 people die giving birth around the world. A leading cause is obstructed labor, often due to the baby’s head exceeding the size of the birth canal. Even successful births require fetal acrobatics to navigate the narrow path from womb to world: Babies typically enter the pelvis sideways, twist, and rotate as they emerge.

Anthropologists have long assumed such perilous births evolved through a tug-of-war between two demands: large brains and upright walking, which favors a pelvis that’s scrunched front to back.  

Difficult births are not unique to humans, however. 

© 2026 American Association for the Advancement of Science. </description>
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<title>Babies born to anaemic mothers have smaller brains,</title>
<link>https://www.theguardian.com/global-development/2026/sep/09/babies-born-to-anaemic-mothers-have-smaller-brains-study-finds</link>
<description>
Kat Lay, Global health correspondent

Babies born to mothers with anaemia have smaller brains, particularly in key regions linked to movement, learning and the regulation of emotion, according to a study.

Researchers said the differences, first detected at the age of one, could lead to cognitive problems when children started school.

More than a third of pregnant women worldwide have anaemia – a condition typically caused by iron deficiency in which the number of red blood cells in the body is lower than normal. Symptoms include fatigue, shortness of breath and dizziness. Rates are highest in sub-Saharan Africa and south Asia.

Researchers from King’s College London in the UK, and the University of Cape Town in South Africa, followed more than 300 mothers and their babies in Cape Town, scanning the brains of the infants several times between the ages of three months and two years.

On average, the total brain volume of babies born to anaemic mothers was 4% lower than that of babies born to non-anaemic mothers – despite all the anaemic mothers being diagnosed only with a mild version of the condition.

Differences were recorded in three specific regions of the brain: the putamen, caudate nucleus and corpus callosum.

“All three of these brain regions are implicated in key neuropsychological functions,” said Jessica Ringshaw, first author and researcher at King’s Institute of Psychiatry, Psychology &amp; Neuroscience (IoPPN) and the University of Cape Town, citing processing speed, emotion regulation and executive function as examples.

© 2026 Guardian News &amp; Media Limited </description>
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<title> New clues suggest how destructive immune cells wreak havoc in the brain</title>
<link>https://www.science.org/content/article/new-clues-suggest-how-destructive-immune-cells-wreak-havoc-brain</link>
<description>
 By Jennie Erin Smith 

A few years ago, scientists saw something surprising in the brain tissue of people who died with Alzheimer’s disease: white blood cells that multiply in response to foreign threats and are seldom seen inside healthy brains.

Whether these so-called CD8+ killer T cells, which normally target infected cells in the body, were there to harm or help was unclear. An answer began to emerge in 2023, when a team led by neuroscientist David Holtzman showed that in mice bred to overexpress tau—a toxic protein that builds up in the neurons of people with Alzheimer’s and several other neurodegenerative diseases—getting rid of the T cells stemmed tissue loss and preserved the mice’s cognition, even as tau kept building up.

Now, the same group has explored what prompts these cells to wreak havoc in the brain. In a mouse study published last week in Nature Neuroscience, Holtzman and immunology researcher Hao Hu, both at Washington University in St. Louis, report that immune cells in the lymph nodes of the neck instruct the T cells to clone themselves before they enter the brain. Without them, the mice had far fewer cloned T cells inside their brains and experienced less neurodegeneration. The study is “beautiful work,” says neuroscientist Kenneth Kosik of the University of California, Santa Barbara, who studies tau but was not involved in the research. It also suggests that existing drugs, developed for other conditions, might work in Alzheimer’s by shielding the brain from the destructive cells.

The new study homes in on a type of dendritic cells, immune cells that, in effect, give the killer T cells their orders. After cutting up the invader’s proteins, the dendritic cells present the antigens as bite-size pieces that T cells can recognize. T cells with compatible receptors can then become activated, which causes the cells to start to clone themselves, attack cells bearing the antigen, and cause inflammation.

© 2026 American Association for the Advancement of Science. </description>
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<title> Fruit flies use memory to track odors</title>
<link>https://www.thetransmitter.org/olfaction/fruit-flies-use-memory-to-track-odors/</link>
<description>
By Calli McMurray

When bats use echolocation to find an object, they don’t point their sonar beam directly at the target, where the intensity of the signal bouncing back would be the strongest. Instead, they aim slightly off axis, so the returning beam contains sharper signal differences. The research team that observed this in 2010 predicted that the same strategy would apply to scent tracking. 

That prediction was correct, a paper published in July in Nature shows. When fruit flies catch a whiff of apple cider vinegar, they zigzag along the edge of the odor plume, where the concentration difference is sharpest, rather than traveling through the middle, where a stronger concentration is likely to hold steady. 

“The edge of the plume is potentially where some of the most information might be stored,” says Marie Suver, assistant professor of biological sciences at Vanderbilt University, who was not involved in the work. “Whereas if you’re in the middle of the plume, you’ll be getting more packets of odor, but it’s not as stark of a concentration gradient as at the edge.”

Keeping tabs on a plume is also more complex than researchers previously thought. When flies and other insects first encounter an odor, they surge upwind and cast side to side when they lose the trail—a behavior that seemed to be a simple reflex, says Matthieu Louis, associate professor of molecular, cellular and developmental biology at the University of California, Santa Barbara, who was not involved in the study. 

“It was supposed to be a memoryless system,” says study investigator Vanessa Ruta, professor and head of the Laboratory of Neurophysiology and Behavior at Rockefeller University. “Basically, all the animal needed to know was the exact sensory experience and information it had at that one moment, and nothing about its prior history would be relevant.”

© 2026 Simons Foundation
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