Wednesday, May 07, 2025

Vehicle age and driver assistance technologies in fatal crashes involving teen and middle-aged drivers



JAMA Network Open



About The Study: 

The findings of this study suggest that older vehicles and those with fewer driver assistance technologies are associated with increased risk of driver death in fatal crashes; thus, teens should drive the safest vehicles available, not older family cars. The findings underscore the urgent need to ensure teens drive safer vehicles to protect their lives.

Corresponding Author: To contact the corresponding author, Jingzhen Yang, PhD, MPH, email ginger.yang@nationwidechildrens.org.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamanetworkopen.2025.8942)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

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About JAMA Network Open: JAMA Network Open is an online-only open access general medical journal from the JAMA Network. On weekdays, the journal publishes peer-reviewed clinical research and commentary in more than 40 medical and health subject areas. Every article is free online from the day of publication. 

 

Reporting and representation of race and ethnicity in clinical trials of pharmacotherapy for mental disorders



JAMA Psychiatry


About The Study: 

The findings of this meta-analysis suggest that differences in reporting race and ethnicity across geographic locations and underrepresentation of certain racial and ethnic groups in U.S.-based randomized clinical trials highlight the need for international guidelines to ensure equitable recruitment and reporting in clinical trials. 

Corresponding Author: To contact the corresponding author, Alessio Bellato, PhD, email a.bellato@soton.ac.uk.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(10.1001/jamapsychiatry.2025.0666)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

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Embed this link to provide your readers free access to the full-text article 

https://jamanetwork.com/journals/jamapsychiatry/fullarticle/10.1001/jamapsychiatry.2025.0666?guestAccessKey=6a7e637c-9712-4ad0-8e5e-8d7804f08e15&utm_source=for_the_media&utm_medium=referral&utm_campaign=ftm_links&utm_content=tfl&utm_term=050725

 

Clinical and neuropathological evaluations of the New Brunswick neurological syndrome of unknown cause



JAMA Neurology



About The Study: There was no evidence supporting a diagnosis of neurological syndrome of unknown cause (NSUC) in this cohort. The data inclusive of independent examinations and neuropathology strongly supported the presence of several neurodegenerative and non-neurodegenerative conditions. Unfounded concerns that a potentially fatal mystery disease, possibly induced by an environmental toxin, is causing the patients’ neurological symptoms has been amplified in traditional and social media. Second, independent clinical evaluations are needed for any patient given a diagnosis of NSUC.


Corresponding Author: To contact the corresponding author, Anthony E. Lang, MD, email anthony.lang@uhn.ca.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamaneurol.2025.1718)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

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 https://jamanetwork.com/journals/jamaneurology/fullarticle/10.1001/jamaneurol.2025.1718?guestAccessKey=f0ce6d56-973c-4c47-922b-ba20bb733830&utm_source=for_the_media&utm_medium=referral&utm_campaign=ftm_links&utm_content=tfl&utm_term=050725

 

Neuroscientists pinpoint where (and how) brain circuits are reshaped as we learn new movements


Discovery of physical modifications across brain regions holds important clues for possible new therapies for brain disorders



University of California - San Diego

Neuronal activity 

image: 

Neuronal activity traces reveal how brain circuits evolve as mice learn a motor task. Left: example field of view recorded during behavior; each color marks a different neuron. Right: activity traces from selected neurons.

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Credit: Komiyama Lab, UC San Diego




A landmark study published by scientists at the University of California San Diego is redefining science’s understanding of the way learning takes place. The findings, published in the journal Nature and supported by the National Institutes of Health and U.S. National Science Foundation, provide novel insights on how brain wiring changes during learning periods, offering a path to new therapies and technologies that aid neurological disorders.

For many years, neuroscientists have isolated the brain’s primary motor cortex (M1), an area in the frontal lobe region, as a hub for sending out signals related to complex movements during episodes of learning. More recently, the motor thalamus, located in the center of the brain, has been implicated as an area that influences M1 during motor learning functions.

But even with such advancements, evidence was lacking on how this learning process unfolds, mainly due to the complex nature of monitoring the interactions of cells across brain areas.

A research team led by Professor Takaki Komiyama’s laboratory used powerful neurobiological research techniques to describe these mechanisms in mice for the first time. Using high-tech imaging and a novel data analysis method, the researchers identified the thalamocortical pathway, a communication bridge between the thalamus and the cortex, as the key area that is modified during learning.

Beyond identifying the main pathway, the researchers found that links between regions physically change during learning. Motor learning does much more than adjust activity levels, it sculpts the circuit’s wiring, refining the conversation between the thalamus and cortex at a cellular level.

“Our findings show that learning goes beyond local changes — it reshapes the communication between brain regions, making it faster, stronger and more precise,” said Assaf Ramot, the study’s lead author and a postdoctoral scholar in the Komiyama Lab. “Learning doesn’t just change what the brain does — it changes how the brain is wired to do it.”

The study, during which mice learned specific movements, revealed that learning causes a focused reorganization of the thalamus and cortex interaction. During times of learning, the thalamus was found to activate M1 neurons to encode the learned movement and to halt the activation of neurons not involved with the movement being learned.

“During learning, these parallel and precise changes are generated by the thalamus activating a specific subset of M1 neurons, which then activate other M1 neurons to generate a learned activity pattern,” said Komiyama, a professor in the Departments of Neurobiology (School of Biological Sciences) and Neurosciences (School of Medicine), with appointments in the HalıcıoÄŸlu Data Science Institute (School of Computing, Information and Data Sciences) and Kavli Institute for Brain and Mind.

To bring the activity of specific neurons into focus — a key insight of the study — the researchers developed a novel analytical method called ShaReD (Shared Representation Discovery) with Neurobiology Assistant Professor Marcus Benna and graduate student Felix Taschbach, study coauthors.

According to Taschbach, who spearheaded development of the data analysis procedure, identifying behaviors that are commonly encoded across different subjects presents a significant challenge because behaviors and their neural representations can vary substantially between animals. To address this issue, the researchers developed ShaReD, which identifies a single shared behavioral representation that correlates with neural activity across different subjects, allowing them to map subtle behavioral features to the activity of different neurons in each animal.

Existing methods typically enforce artificial alignment to reduce individual variability — similar to requiring everyone to follow exactly the same route to a destination. In contrast, ShaReD functions more like identifying which landmarks consistently help travelers navigate, regardless of their specific route choices. The ShaReD method was critical to the study’s findings.

“This new method allows us to combine data from multiple experiments to make detailed discoveries that would not have been possible using only the limited number of relevant neurons recorded in an individual brain,” said Benna, a computational neuroscientist and co-corresponding author of this study.

The new study is the second recently led by the Komiyama lab that illuminates how our brains learn. In April, William Wright, Nathan Hedrick and Komiyama published a study in Science that describes the multiple rules that neurons follow during episodes of learning, with synapses in different regions following different rules.

With the Nature study’s findings, the researchers further science’s understanding of the learning process with a new comprehensive model of how the neural circuits underlying learned movements emerge during learning. The new information also offers hope for those who suffer from neurological disorders.

“The study shows that learning isn’t just repetition,” said Ramot. “It’s about your brain literally rewiring itself in a targeted way. Whether you’re learning a new skill, recovering from a stroke or using a neuroprosthetic, understanding how brain regions reorganize their communication helps us design better therapies and technologies that work with the brain’s natural learning mechanisms.”

The paper is dedicated to the memory of An Wu, an assistant project scientist in Komiyama’s lab who tragically died in a 2023 Montreal building fire. She is remembered as a brilliant neuroscientist who elevated the many lives she touched.

 

Scientists map tongue’s sweet sensor, may lead to new ways to curb sugar cravings



Discovery reveals the workings of the key molecule responsible for our insatiable attraction to sugar.


The Zuckerman Institute at Columbia University

Scientists Map Tongue’s Sweet Sensor, May Lead to New Ways to Curb Sugar Cravings 

video: 

Cryo-EM map of the human sweet taste receptor (blue and green) changing shape as it binds a molecule that tastes sweet (red and green).

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Credit: J. Zhang et al.




NEW YORK — Our attraction to sugar has grown to an unhealthy level. The average person in the United States now consumes more than 100 pounds of the sweet stuff every year, up from 18 pounds in 1800.

With new research published May 7, in Cell, Columbia University scientists have taken a major step toward dealing with this public health crisis. For the first time, they have mapped the 3-D structure of the human sweet taste receptor, the molecular machine that allows us to taste sweet things. This could lead to the discovery of new regulators of the receptor that would significantly alter our attraction to and appetite for sugar.

"The leading role that sugar plays in obesity cannot be overlooked," said study co-first author Juen Zhang, PhD, a postdoctoral fellow in the lab of Charles Zuker, PhD, at Columbia’s Zuckerman Institute and at the Howard Hughes Medical Institute. “The artificial sweeteners that we use today to replace sugar just don’t meaningfully change our desire for sugar. Now that we know what the receptor looks like, we might be able to design something better.”

The sweet receptors on our tongue can detect a large number of different chemicals that taste sweet, from common table sugar (also known as sucrose) to antimicrobial enzymes in chicken eggs. Unlike other receptors—for bitter, sour, or other tastes—our sweet sensors evolved to not be very sensitive. This helps us focus on sugar-rich foods for energy, and drives a need for a lot of sweets to satisfy our sweet tooth.

Determining the structure of the human sweet receptor is key to comprehending how it helps us detect sweet taste, fundamentally advancing our understanding of taste perception. More than 20 years ago, Dr. Zuker and his colleagues uncovered the genes behind the mammalian sweet taste receptor. This landmark work revealed its chemical formula, but until now no one knew its precise shape, much like how knowing a cake's recipe will not tell you what the pastry will look like when finished.

Without this knowledge, understanding the molecular basis of sweet detection to rationally design ways to regulate the function of this essential receptor has been a challenge, said Dr. Zuker, in whose laboratory this new work was also carried out.

 "All the artificial sweeteners that we use today were either discovered by accident or based on known sweet-tasting molecules," said study co-author Brian Wang, a research assistant in the Zuker lab. "As a result, most artificial sweeteners have drawbacks.”

The new work maps the structure of the human sweet taste receptor in unprecedented detail, to a resolution as good as 2.8 angstroms. In comparison, the smallest atom, hydrogen, is slightly more than 1 angstrom wide.

It took the researchers innovative approaches and about three years to map the human sweet taste receptor's structure, in large part because it proved difficult to grow this protein on cells in lab dishes. 

“Just getting the purified protein we needed to map the structure took more than 150 different preparations over the course of three years," said study co-first author Zhengyuan Lu, a doctoral student at the Zuker lab. 

The scientists then used cryo-electron microscopy (cryo-EM) to analyze the human sweet taste receptor. This technique fires beams of electrons at molecules that have been frozen in solution, helping researchers capture snapshots of those molecules from different perspectives, from which they can reconstruct their three-dimensional structures at the atomic level.

Of particular importance, cryo-EM revealed the receptor’s binding pocket: the cavity where sweet things stick and trigger the set of reactions that drive our strong appetite for sweets.

"Defining the binding pocket of this receptor very accurately is absolutely vital to understanding its function," said study co-author Anthony Fitzpatrick, PhD, a principal investigator at Columbia’s Zuckerman Institute. “By knowing its exact shape, we can see why sweeteners attach to it, and how to make or find better molecules that activate the receptor or regulate its function,” added Dr. Fitzpatrick, who is also an assistant professor of biochemistry and molecular biophysics at Columbia’s Vagelos College of Physicians and Surgeons.

The human sweet taste receptor consists of two main halves. One of these, named TAS1R2, possesses the binding pocket, a component resembling a Venus flytrap. Knowing the structure of this part may also help us understand why people differ in how sensitive they are to sweets.

The scientists mapped the receptor's structure as it bound to two of the most commonly used artificial sweeteners, aspartame and sucralose. These are, respectively, 200 and 600 times sweeter than sucrose.

The researchers then systematically altered tiny parts of the receptor. This helped shed light on the role each of these parts play in binding onto the sweeteners, said study co-author Ruihuan Yu, a doctoral student at the Zuker lab. 

"We're trying to move our understanding of science forward to be able to help people," said study co-author Andrew Chang, a research technician at the Fitzpatrick lab.

Although the human sweet taste receptor is found mostly on taste buds in the mouth, Dr. Zhang noted it is also scattered throughout the body, where it may play a role in the function of organs such as the pancreas. As such, the new map of this receptor’s structure might support research investigating our metabolism, as well as in disorders such as diabetes. 

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The paper, "The structure of human sweetness," was published in Cell on May 7, 2025.

The full list of authors includes Juen Zhang, Zhengyuan Lu, Ruihuan Yu, Andrew N. Chang, Brian Wang, Anthony W.P. Fitzpatrick and Charles S. Zuker.

The authors report no competing interests.