A study published in Molecular Psychiatry suggests that the biology underlying autism and ADHD does not fit neatly into current diagnostic categories. Although clinicians have long recognized that autism and ADHD frequently occur together, scientists have struggled to pinpoint the shared mechanisms behind that overlap.

Researchers from the Child Mind Institute and collaborating centers found that the intensity of autism symptoms, rather than whether a child carries a diagnosis of autism spectrum disorder (ASD) or attention-deficit/hyperactivity disorder (ADHD), is linked to specific patterns of brain connectivity and gene activity. The results add to a growing shift in psychiatry toward understanding neurodevelopmental conditions along dimensions of traits and biology, rather than as strictly separate disorders.

Symptom severity reveals shared biology
The research team, led by Adriana Di Martino, MD, Founding Director of the Autism Center at the Child Mind Institute and Senior Research Scientist, analyzed resting-state functional MRI scans from 166 verbal children between the ages of 6 and 12 who had been diagnosed with autism or ADHD (without autism). Resting-state imaging allows scientists to measure how different brain regions communicate while a person is not engaged in a specific task, offering insight into underlying network organization.

Children with more pronounced autism symptoms showed stronger connectivity between regions in the frontoparietal (FP) and default-mode (DM) networks. These networks play central roles in executive functioning, attention, and social cognition. In typical development, connectivity between these networks tends to decrease over time as the brain becomes more specialized. The heightened connectivity observed in children with greater symptom severity suggests differences in how these networks mature.

Importantly, this pattern appeared across the full group of children, regardless of whether they were formally diagnosed with ASD or ADHD. The connectivity differences also aligned with maps of gene expression in the brain, particularly genes involved in neural development that have previously been linked to both conditions. This overlap points to biological pathways that may cut across diagnostic labels.

“We see in the clinic that some children with ADHD share symptoms qualitatively similar to those observed in autism, even if they do not fully meet the diagnostic criteria for ASD,” says Dr. Adriana Di Martino. “By focusing on shared brain–gene expression patterns linked to autism symptoms across both ASD and ADHD, we can point towards a shared biological basis of these clinical observations. Our findings provide a more nuanced, dimensional understanding of neurodevelopmental conditions.”

Australian scientists have uncovered strong evidence that chronic insomnia may stem from disruptions in the brain’s internal 24-hour cycle of mental activity. The findings help explain why some people find it so difficult to “switch off” at night, even when they are physically tired.

In a study published in Sleep Medicine, researchers from the University of South Australia (UniSA) tracked how thinking patterns rise and fall across the day in people with long-term insomnia compared with healthy sleepers. This is the first study to chart daily cognitive rhythms in this way.

Insomnia affects roughly 10% of the population and up to one-third of older adults. Many people with the condition describe their minds as overactive or constantly racing at night.

Although this nighttime mental alertness has often been described as cognitive hyperarousal, its underlying cause has remained uncertain. The researchers set out to test whether difficulty calming the mind at night, a defining feature of insomnia, might be linked to abnormalities in circadian rhythms, the body’s internal timekeeping system.

Scientists at the Kunming Institute of Zoology (KIZ) of the Chinese Academy of Sciences have shown for the first time in non-human primates that sound stimulation at 40-Hz can significantly increase β-amyloid levels in the cerebrospinal fluid (CSF) of aged rhesus monkeys. Notably, this effect lasted for more than five weeks after treatment ended.

The findings, published in PNAS, provide the first experimental evidence in non-human primates that 40-Hz stimulation could serve as a non-invasive physical approach for Alzheimer’s disease (AD). The study also highlights important differences between primate and rodent models, which are often used in preclinical research.

Led by Dr. Xintian Hu at KIZ, the research team worked with nine elderly rhesus macaques (Macaca mulatta) between 26 and 31 years old. These monkeys naturally developed widespread amyloid plaques in their brains, closely resembling the Aβ pathology seen in human AD. Because of this similarity, they offer a valuable model for testing potential therapies before moving to human trials.

Webb maps the mysterious upper atmosphere of Uranus 🔵

This first vertical view of its ionosphere reveals auroras shaped by the planet's tilted magnetic field and how Uranus’s atmosphere has continued to cool over the past three decades.

Read more 👉 esa.int/Science_Explor…

Scientists at Osaka Metropolitan University in Japan have identified a new and unexpected behavior in cleaner wrasse (Labroides dimidiatus). When shown a mirror, these small reef fish did more than appear to recognize their reflections. They also began interacting with the mirror using a piece of food, suggesting a level of cognitive sophistication not typically associated with fish. The findings indicate that cleaner wrasse may be capable of “contingency testing,” a complex mental process most often observed in highly intelligent marine mammals such as dolphins.

The research team was led by Specially Appointed Researcher Shumpei Sogawa and Specially Appointed Professor Masanori Kohda at the Graduate School of Science. In earlier work, the group demonstrated that cleaner wrasse can identify themselves in photographs.

In the current study, the scientists observed new behaviors during a series of mirror test experiments, a widely used method for evaluating self-recognition and animal cognition. Previous research had already shown that cleaner wrasse respond to their reflections in ways consistent with self-recognition.

In the critical hours after an offshore oil spill, response teams must make a difficult choice: allow the slick to spread or set it on fire.

When responders ignite the oil, they create what is known as an ‘in-situ’ fire pool. This method can prevent oil from drifting and contaminating fragile marine ecosystems — but it comes at a heavy cost. Thick smoke rises into the air, soot and other pollutants spread through the atmosphere, and a layer of partially burned residue remains on the ocean surface.

In a first-of-its-kind large-scale experiment, scientists tested a different strategy: enormous fire whirls, spinning columns of flame that rise vertically like a tornado instead of spreading across the water.

Fire Whirls: A Cleaner, Faster Oil Spill Solution
This rotating column acts like a powerful engine. As it spins, it pulls in extra oxygen, which allows the flame to burn hotter and more efficiently than a traditional fire pool.

The improvement was dramatic. Compared with standard in-situ fires, the fire whirl generated 40 percent less soot and burned up to 95 percent of the oil, leaving behind far fewer hazardous particles and toxic remnants.

For decades, researchers have recognized that Alzheimer’s disease is marked by the buildup of toxic protein fragments in the brain. What has remained unclear is exactly how and where those harmful fragments are generated.

In a new study, scientists at Northwestern University report that they have identified both the location and timing of this toxic buildup in Alzheimer’s patients. The team also found that an inexpensive drug already approved by the Food and Drug Administration (FDA) can interrupt the process before the damage begins.

Using a combination of animal models, lab-grown human neurons, and brain tissue from individuals at high risk for Alzheimer’s, the researchers focused on a particularly harmful fragment known as amyloid-beta 42. They discovered that this peptide accumulates inside synaptic vesicles, the small sacs neurons use to release chemical signals and communicate with one another.

When the scientists treated animals and human neurons with levetiracetam, a widely prescribed anti-seizure medication that has been available for decades, the drug blocked the formation of amyloid-beta 42. By preventing production of the peptide, levetiracetam stopped the chain of events that leads to amyloid plaque buildup.

“While many of the Alzheimer’s drugs currently on the market, such as lecanemab and donanemab, are approved to clear existing amyloid plaques, we’ve identified this mechanism that prevents the production of the amyloid-beta 42 peptides and amyloid plaques,” said corresponding author Jeffrey Savas, PhD, associate professor of behavioral neurology at Northwestern University Feinberg School of Medicine. “Our new results uncovered new biology while also opening doors for new drug targets.”

Researchers have uncovered specific biological changes in taste buds that could help explain why a small number of people continue to struggle with taste loss long after a COVID-19 infection.

The study, published in Chemical Senses, is the first to directly connect patients’ lingering taste complaints with measurable abnormalities inside the cells responsible for detecting flavor.