Hebrew University of Jerusalem

By Pesach Benson and Omer Novoselsky • January 12, 2026

Jerusalem, 12 January, 2026 (TPS-IL) — Some women’s breast cells may show signs of future cancer years before any tumor appears, potentially helping doctors detect breast cancer much earlier — or perhaps even prevent it from developing, the Hebrew University of Jerusalem announced.

On average, one in twenty women globally will be diagnosed with breast cancer, according to the World Health Organization.

A team of Israeli and U.S. scientists opened a previously hidden window into how breast cancer begins in women carrying BRCA1 or BRCA2 mutations. The research shows that even before tumors appear, breast cells in BRCA mutation carriers already exhibit a distinct pattern of DNA “damage spots” that closely resemble the DNA break patterns seen in cancer cells.

The study was led by PhD student Sara Oster Flayshman under the guidance of Professor Rami Aqeilan and Dr. Yotam Drier at Hebrew University’s Faculty of Medicine, in collaboration with Dr. Victoria Seewaldt and Dr. Mark LaBarge from the City of Hope research center in California. Using next-generation sequencing, the team mapped DNA double-strand breaks (DSBs) across the genomes of non-malignant mammary epithelial cells from women carrying high-risk genetic mutations.

The team found that the pattern of DNA damage in these cells was very different from what they saw in healthy cells and, surprisingly, looked much like the patterns found in breast cancer cells. The most affected DNA regions were those linked to cancer, especially the ones that are normally very active in the cell, making them more likely to lead to cancer if damaged.

The study was recently published in the peer-reviewed journal Cell Death & Disease.

Professor Aqeilan told The Press Service of Israel that the study’s significance lies in the early, pre-cancerous cellular instability.

“Our main finding is that non-malignant mammary epithelial cells from high-risk women already show a distinct, non-random ‘breakome’ compared with average-risk controls and, importantly, this breakome partly resembles the pattern seen in breast cancer cells,” he said. A breakome refers to the complete pattern or map of DNA breaks across a cell’s genome.

“This suggests that genome instability–related processes are underway very early, before any tumor is present, and that these early weaknesses can reshape where DNA breaks accumulate,” said Aqeilan.

The researchers emphasized that the DNA break patterns are detectable in young, cancer-free donors, including women under 35. “That means the shift is detectable well before clinical cancer, and plausibly years, potentially decades, before diagnosis for carriers who develop disease later,” Aqeilan said. While the study does not provide a precise lead time to cancer onset, it challenges the traditional view that loss-of-heterozygosity (LOH) events are the first step in malignancy.

The study opens potential avenues for early detection.

“This work provides critical insight into the earliest molecular changes that take place in breast cells of high-risk women,” Aqeilan told TPS-IL. “Understanding these initial events allows us to envision new strategies for identifying cancer at its earliest, most treatable stages.”

Drier noted that these patterns “could one day help us develop more precise biomarkers, so that high-risk women are not only monitored more effectively, but also offered interventions based on the actual biology of their cells.”

While the current study focuses on breast tissue, Aqeilan said the next steps will explore whether similar patterns emerge in other cancer-prone tissues.

“Testing ovarian and fallopian tissue is explicitly a logical next step,” he told TPS-IL.

In addition, his team plans to study larger groups of women over time to see whether early DNA damage patterns can predict who will eventually develop cancer, and to explore minimally invasive tests that could detect these patterns before tumors form.

Understanding these early DNA breaks may also shed light on why some high-risk women develop cancer while others do not. “It could guide new prevention strategies that target these vulnerable regions of the genome before cancer starts,” Aqeilan said.

By Pesach Benson • January 8, 2026

Jerusalem, 8 January, 2026 (TPS-IL) — Israeli scientists have developed a new 3D-printed solar panel that is both semi-transparent and color-tunable, offering a flexible alternative to conventional solar technology, the Hebrew University of Jerusalem announced. The breakthrough could allow buildings to generate electricity without sacrificing natural light or aesthetic appeal, potentially transforming the way cities harness solar power.

The study, led by Prof. Shlomo Magdassi and Prof. Lioz Etgar from the university’s Institute of Chemistry and the Center for Nanoscience and Nanotechnology, introduces a solar cell design that produces electricity while allowing architects and designers to control both how much light passes through and the color of the panels.

“At the heart of the design is a pattern of microscopic polymer pillars created using 3D printing,” Prof. Magdassi explained. “Our goal was to rethink how transparency is achieved in solar cells. By using 3D-printed polymer structures made from non-toxic, solvent-free materials, we can precisely control how light moves through the device in a way that is scalable and practical for real-world use.”

The tiny pillars act like carefully shaped openings that regulate light transmission without altering the solar material itself. The method also avoids high temperatures and toxic solvents, making it suitable for flexible surfaces and environmentally friendly production — a key consideration for architects and urban planners looking to integrate solar technology seamlessly into buildings.

Prof. Etgar highlighted the design’s visual flexibility. “What’s especially exciting is that we can customize both how the device looks and how flexible it is, without sacrificing performance. That makes this technology particularly relevant for solar windows and for adding solar functionality to existing buildings.” By adjusting the thickness of a transparent electrode layer, the panels can reflect selected wavelengths of light, producing different colors while continuing to generate electricity.

Laboratory tests showed power conversion efficiencies, of up to 9.2 percent, with roughly 35 percent visible transparency. The cells also maintained performance after repeated bending and extended operation, demonstrating durability essential for real-world architectural use.

Looking ahead, the researchers plan to enhance long-term durability through protective encapsulation and barrier layers.

Beyond the laboratory, the team envisions a range of real-world applications that could bring this flexible, color-tunable solar technology into everyday architecture and urban design.

The semi-transparent, color-tunable solar panels could transform how buildings generate electricity. They can be integrated into windows, glass walls, and façades, allowing offices, homes, and commercial spaces to produce power without blocking natural light or compromising design. Their flexibility also makes them suitable for curved or unconventional surfaces that traditional rigid panels cannot cover, opening the door to more creative and functional architectural designs.

Beyond new construction, the technology could retrofit existing buildings, adding solar functionality without major renovations. Color customization lets designers seamlessly match panels to a building’s aesthetic, while lightweight and flexible construction could extend applications to temporary structures or even portable devices. Combined with environmentally friendly manufacturing that avoids high heat and toxic solvents, these solar cells offer a practical, scalable solution for sustainable energy in urban and architectural environments.

The study was published in the peer-reviewed EES Solar journal.

By Pesach Benson and Omer Novoselsky • January 7, 2026

Jerusalem, 7 January, 2026 (TPS-IL) — An international team of scientists has identified hundreds of genes that are essential for early brain development, uncovering new insights into the biological roots of neurodevelopmental disorders, including autism, and describing a previously unknown genetic condition that disrupts brain growth, the Hebrew University of Jerusalem announced.

The study, published in the peer-reviewed journal Nature Neuroscience, used large-scale CRISPR gene-editing technology to systematically determine which genes are required as embryonic stem cells developed into brain cells.

Led by Prof. Sagiv Shifman of Hebrew University’s Institute of Life Sciences in collaboration with Prof. Binnaz Yalcin of INSERM in France, the team of Israeli, French and Japanese scientists set out to answer a fundamental question in neuroscience: which genes are necessary for building a healthy brain, and what happens when that process fails?

Using a genome-wide CRISPR knockout screen, the researchers individually disabled nearly 20,000 genes in embryonic stem cells as they transitioned into neural cells. This allowed the team to observe, step by step, which genes were indispensable for normal neural differentiation. In simple terms, neural differentiation is how a generic early cell learns to become a brain or nerve cell. Through this approach, the scientists identified 331 genes that are essential for generating neurons, many of which had not previously been linked to brain development.

While the findings span a wide range of neurodevelopmental conditions, the implications for autism stood out in both the data and in The Press Service of Israel’s interview with Shifman. The study’s results suggest that not all neurodevelopmental disorders arise from the same types of genetic disruptions, and that timing during brain development plays a critical role.

Autism Risk Genes Emerge

“The study delivers a genome-wide, stage-resolved essentiality map of neural differentiation,” Shifman told TPS-IL. “By knocking out about 20,000 genes during the transition from embryonic stem cells to neural lineages, we identified 331 genes required for neuronal generation and showed how this map can both interpret human genetic risk and help discover new neurodevelopmental disease genes.”

According to the study, genes that are broadly essential for basic cellular survival tend to be associated with more global developmental delay. In contrast, genes that are especially critical at specific stages of nerve cell formation show a stronger association with autism. This distinction helps explain why autism often presents differently from other neurodevelopmental disorders, even when symptoms overlap.

“It supports a timing-based view of autism risk,” Shifman told TPS-IL. “Autism-associated genes are enriched among those that are particularly critical at specific steps of nerve cell formation, as opposed to those needed broadly for basic cellular viability. This suggests that autism genes are involved in early developmental processes required for generating neural progenitors and neurons.”

The dataset includes both known and previously unrecognized autism-related genes. While roughly 100 of the 331 essential genes had already been implicated in neurodevelopmental disorders, the majority represent new candidates for further study. “Only a minority of the essential genes we identified are currently implicated in neurodevelopmental disorders,” Shifman told TPS-IL. The findings significantly expand the pool of genes researchers can investigate.

New Brain Disorder Identified

Beyond autism, the study also describes a new neurodevelopmental disorder linked to mutations in the gene PEDS1. This gene is required for the production of plasmalogens, specialized membrane lipids that are abundant in myelin, the insulating layer around nerve fibers. In the CRISPR screen, PEDS1 emerged as crucial for nerve cell formation, with its loss leading to reduced brain size.

Genetic analyses of two unrelated families revealed rare PEDS1 mutations in children with severe developmental delay and abnormally small brains. Follow-up experiments confirmed that inactivating PEDS1 disrupts normal brain development, including the generation and migration of neurons, providing a clear mechanistic explanation for the clinical features observed.

In addition to identifying disease genes, the research sheds light on inheritance patterns. The team found that genes involved in regulating transcription and chromatin are more often linked to dominant disorders, where a mutation in a single gene copy is sufficient to cause disease. Metabolic genes, such as PEDS1, are more commonly associated with recessive disorders that require mutations in both copies of the gene. This relationship could help clinicians prioritize candidate genes when interpreting genetic test results.

The researchers have also made their findings widely accessible by launching an open online database that includes the full results of the CRISPR screen. Shifman credited PhD student Alana Amelan with driving the initiative. “We wanted our findings to serve the entire scientific community,” he explained.

Looking ahead, Shifman said the essentiality map will serve as a platform for future discoveries. “The natural next step is to use the essentiality map as a discovery platform,” he told TPS-IL, adding that his lab is now focusing on the mechanisms of specific autism genes, sex differences in diagnosis, and the biological basis of autism’s wide clinical diversity.

By Pesach Benson • January 4, 2026

Jerusalem, 4 January, 2026 (TPS-IL) — A new Israeli study is challenging one of the most entrenched assumptions in microbiology: that bacteria survive antibiotics primarily by going dormant. The research shows that antibiotic persistence is not a single biological phenomenon, but instead arises from two fundamentally different growth-arrest states, a discovery that helps resolve years of contradictory findings and opens new paths for preventing recurring infections.

Antibiotics are designed to eliminate bacteria by disrupting processes tied to growth and division. Yet in many infections, a small subset of bacterial cells survives treatment and later reignites disease. This phenomenon, known as antibiotic persistence, is a major cause of treatment failure and relapse, even when bacteria show no genetic resistance to the drugs.

For decades, persistence was largely attributed to dormancy, the idea that bacteria shut down growth in a regulated way, entering a stable, sleep-like state that shields them from antibiotics. But new research at the Hebrew University of Jerusalem, led by PhD student Adi Rotem under the supervision of Prof. Nathalie Balaban, shows that this explanation captures only part of the reality.

The study demonstrates that high survival under antibiotics can originate from two distinct physiological states, not merely variations of dormancy. One state fits the classic model of regulated growth arrest, in which bacteria actively slow their metabolism and maintain internal stability. The other is fundamentally different: a disrupted, dysregulated growth arrest, in which cells survive by slipping into a malfunctioning state rather than a controlled shutdown. The findings were recently published in the peer-reviewed Science Advances journal.

“We found that bacteria can survive antibiotics by following two very different paths,” said Balaban. “Once you recognize that these are distinct states, many of the contradictions in the literature suddenly make sense.”

In the regulated state, bacteria deliberately enter a protected condition. Because many antibiotics rely on active growth to be effective, these dormant cells are difficult to kill. This mechanism has long dominated thinking about persistence and has shaped experimental approaches across the field.

The disrupted state, however, challenges that paradigm. In this mode, bacteria are not calmly protecting themselves but instead exhibit a widespread loss of cellular control. The researchers found that these cells show impaired membrane homeostasis, a core function required to maintain cell integrity. Despite this dysfunction, the cells can survive antibiotic exposure and later recover, demonstrating that persistence does not require orderly dormancy.

This insight addresses a long-standing problem in persistence research. Over the years, studies have reported conflicting observations about persister cells, describing them as metabolically inactive in some experiments and highly disordered in others. According to the authors, those discrepancies likely arose because researchers were unknowingly studying different growth-arrest states and treating them as a single phenomenon.

“People were often looking for one defining signature of persistence,” the researchers noted, “but what we see is that there are at least two biologically distinct ways bacteria can get through antibiotic treatment.”

The distinction has practical implications. While regulated dormant cells are broadly protected, disrupted cells carry specific vulnerabilities. Their compromised membranes, the study suggests, could be exploited therapeutically, making them susceptible to treatments that would not affect classic dormant persisters.

Antibiotic persistence plays a role in recurring infections ranging from chronic urinary tract infections to infections associated with medical implants. By showing that persistence is not a single target but a set of distinct physiological states, the findings suggest that future therapies may need to be tailored, combining different strategies to eliminate different persister types.

To uncover these differences, the team combined mathematical modeling with high-resolution experimental approaches, including transcriptomics to track gene expression, microcalorimetry to measure metabolic activity through heat output, and microfluidic systems that allowed real-time observation of individual bacterial cells. These methods revealed clear signatures separating regulated and disrupted growth arrest.

As a result of the study, instead of trying to invent one “magic” drug that kills all lingering bacteria, scientists can now design treatments that deal with each survival strategy separately. Some bacteria survive by deliberately slowing down and hiding, while others survive in a damaged, unstable state. Knowing the difference makes it possible to target them more precisely.

Another application is the smarter use of existing antibiotics. Treatments could be combined so that one drug kills actively growing bacteria, another wakes up dormant ones, and a third attacks weakened cells with damaged membranes.

The findings also help explain why some drugs look promising in the lab but fail in real patients. A treatment may work well against one type of surviving bacteria but miss the other. With this new understanding, researchers can test drugs more realistically.

The study also opens the door to new kinds of treatments that do not rely solely on antibiotics. Some of the surviving bacteria are fragile in specific ways, especially in their outer membranes. Therapies that take advantage of those weaknesses could help clear infections without adding to antibiotic resistance.

By Pesach Benson • December 23, 2025

Jerusalem, 23 December, 2025 (TPS-IL) — Doctors have long known that gestational diabetes increases the risk of complications for both mothers and babies, but exactly how it harms the developing fetus has remained unclear. A new study from the Hebrew University of Jerusalem has now identified a previously unknown molecular process in the placenta that may help explain those risks and open new pathways for treatment.

Gestational diabetes mellitus is a form of diabetes that develops during pregnancy and is increasing in prevalence worldwide. It exposes the fetus to an abnormal metabolic environment, including elevated maternal blood glucose levels. The condition is associated with complications such as babies being born too large or too small, higher rates of caesarean and pre-term deliveries, and increased neonatal risks.

In addition, children born to mothers with gestational diabetes also face a higher likelihood of obesity and diabetes later in life.

Because diagnostic criteria and screening practices differ, there is no single global rate, but most estimates place gestational diabetes in about 10–15% of pregnancies worldwide, making it one of the most common pregnancy complications. When gestational diabetes is diagnosed, treatment focuses on controlling blood sugar levels to protect both the mother and the fetus.

The new research shows that gestational diabetes alters a fundamental biological process in the placenta known as RNA splicing. Splicing is the step in which genetic messages are assembled before being translated into proteins. According to the scientists, this is the first evidence that gestational diabetes causes widespread errors in placental RNA splicing, leading to hundreds of incorrectly assembled genetic messages that may impair how the placenta functions.

The study was led by Prof. Maayan Salton of the Faculty of Medicine at the Hebrew University of Jerusalem and Dr. Tal Schiller of the Hebrew University’s Kaplan Medical Center and Wolfson Medical Center at Tel Aviv University, together with PhD students Eden Engal and Adi Gershon. Researchers from other Israeli and European institutions were also involved. The findings were published in the peer-reviewed journal Diabetes.

Using advanced RNA sequencing data from both European and Chinese pregnancy cohorts, the researchers identified hundreds of consistent splicing alterations in placentas affected by gestational diabetes. Many of the affected genes play key roles in metabolism and diabetes-related pathways. The fact that the same molecular changes were observed across distinct populations suggests that disrupted splicing is a core feature of gestational diabetes rather than a secondary or population-specific effect.

A central discovery of the study was the role of a protein called SRSF10, which helps regulate RNA splicing. When the researchers experimentally reduced SRSF10 activity in placental cells, they observed the same splicing errors seen in gestational diabetes. This indicates that SRSF10 is not merely associated with the disease but may actively drive placental dysfunction. The identification of SRSF10 as a key regulator had not previously been linked to gestational diabetes or placental biology.

“By pinpointing the specific molecular players involved, like the SRSF10 protein, we can start thinking about how to translate this knowledge into real-world strategies to improve pregnancy outcomes,” Schiller said.

Gestational diabetes is typically managed through diet, exercise, and insulin, approaches that control blood sugar but do not address underlying placental changes. By uncovering a direct link between maternal metabolism, placental RNA splicing, and fetal risk, the researchers say the study opens new avenues for interventions aimed at reducing both immediate complications and long-term health consequences for children.

First, the findings provide a clear biological explanation for pregnancy and long-term offspring complications that are not fully prevented by glucose control alone. Clinically, many women have well-managed blood sugar, yet their children still face higher metabolic risks. This study suggests that placental molecular dysfunction, not just blood glucose levels, may be driving some of those outcomes.

Second, the research identifies placental RNA splicing as a new therapeutic target. This opens the door to placenta-focused interventions aimed at correcting molecular errors rather than only managing symptoms.

Third, the identification of SRSF10 as a key regulator has practical research and drug-development implications. Because reducing SRSF10 activity reproduced gestational diabetes–like defects in placental cells, the protein could serve as a drug target or a pathway to modulate. Even partial correction of its activity might reduce placental dysfunction and downstream fetal risk.

Fourth, the findings may lead to new biomarkers for risk stratification. Splicing signatures or SRSF10-related molecular changes in placental tissue — or potentially in maternal blood — could help identify pregnancies at higher risk of complications, even when glucose levels appear well controlled.

Fifth, the study supports more personalized management of gestational diabetes. In the long term, clinicians may be able to distinguish between patients whose pregnancies are primarily affected by metabolic imbalance and those with pronounced placental molecular disruption, allowing for tailored monitoring and intervention strategies.

“By understanding how gestational diabetes disrupts the placenta at the molecular level, we can begin to imagine new ways to protect the offspring,” Salton said.

By Pesach Benson • December 18, 2025

Jerusalem, 18 December, 2025 (TPS-IL) — A tiny viral switch discovered by Israeli and American scientists could open a new front in the fight against antibiotic-resistant infections, a global health threat projected to kill up to 10 million people annually by 2050. Scientists at the Hebrew University of Jerusalem have revealed that bacteriophages—viruses that infect bacteria—use a small RNA molecule to hijack bacterial cells, a mechanism that had never been described before, offering fresh insights for future phage-based therapies.

The study, led by Dr. Sahar Melamed and her team, including PhD student Aviezer Silverman, MSc student Raneem Nashef, and computational biologist Reut Wasserman, in collaboration with Prof. Ido Golding from the University of Illinois Urbana-Champaign, focused on a tiny viral RNA called PreS. Unlike most prior research, which concentrated on viral proteins, this study showed that even one of the most studied phages, lambda, uses RNA to directly manipulate bacterial gene expression.

“This small RNA gives the phage another layer of control,” Melamed said. “By regulating essential bacterial genes at exactly the right moment, the virus improves its chances of successful replication. What astonished us most is that phage lambda, studied for more than 75 years, still hides secrets. Discovering an unexpected RNA regulator in such a classic system suggests we have only grasped a single thread of what may be a much richer network of RNA-mediated control in phages.”

The researchers discovered that PreS acts like a molecular “switch” inside infected bacteria, targeting specific bacterial messenger RNAs. One key target is the message that codes for DnaN, a protein essential for DNA replication. PreS binds to a normally folded portion of this mRNA, unfolds it, and makes it easier for the bacterial protein-making machinery to translate it. The result is more DnaN protein, faster viral DNA replication, and a more efficient infection. When PreS is removed or its binding site disrupted, the phage weakens, multiplies more slowly, and its destructive phase is delayed.

“This mechanism had never been seen before in phages,” said Silverman. “It shows that even the smallest viral molecules can play a decisive role in infection, giving the virus a subtle but powerful advantage over its host.”

The discovery is particularly striking because small RNAs were not previously considered major players in phage biology. Yet PreS is highly conserved across related viruses, suggesting that many phages may share a hidden “toolkit” of RNA regulators, a field scientists are only beginning to explore.

Understanding how phages control bacterial cells is crucial for both fundamental biology and potential medical applications. With antibiotic resistance rising worldwide, phage therapy—using viruses to selectively attack bacteria—is gaining attention as a flexible, targeted alternative to conventional drugs. Discoveries like PreS provide a blueprint for designing smarter phages that are safer, more predictable, and more effective in combating drug-resistant infections.

“Even the smallest viral molecules can have a huge impact on whether an infection succeeds,” Melamed said. “By learning how phages manipulate their hosts at this microscopic level, we can begin to engineer viruses that are both powerful and precise in the fight against antibiotic resistance.”

Understanding how PreS manipulates bacterial cells could help scientists design smarter phage therapies that are more efficient at targeting harmful bacteria, particularly strains resistant to antibiotics. By harnessing these RNA-based mechanisms, researchers could develop precision treatments capable of attacking multi-drug-resistant infections that conventional antibiotics cannot touch.

Beyond medicine, the findings may also have applications in synthetic biology, allowing engineered phages or bacteria to be used in industrial processes, microbiome management, or controlling biofilms, turning a once-hidden viral strategy into a versatile tool for both health and technology.

The study was published in the peer-reviewed Molecular Cell journal.

By Pesach Benson • December 17, 2025

Jerusalem, 17 December, 2025 (TPS-IL) — Israeli scientists have developed a new gene-editing method that could significantly improve mosquito control programs by making it easy to distinguish male mosquitoes from females — a longstanding challenge in curbing mosquito-borne diseases, the Hebrew University of Jerusalem announced on Tuesday.

Mosquitoes are among the most dangerous animals to humans, primarily due to their role in spreading disease. Female mosquitoes transmit viruses and parasites when they bite, including Dengue, Zika, Chikungunya, malaria, yellow fever, and West Nile virus. Together, these diseases infect hundreds of millions of people each year.

Only female mosquitoes transmit diseases to humans. Female mosquitoes bite because they need blood proteins to develop their eggs. When they feed, they can pick up viruses or parasites from an infected person or animal and later pass them on to another host through subsequent bites. Male mosquitoes feed on nectar and plant sugars and do not bite.

Currently, mosquito control programs such as the Sterile Insect Technique aim to suppress populations by releasing large numbers of sterile males, which mate with wild females and reduce reproduction. However, existing separation methods typically rely on size differences at the mosquito’s pupal stage, a process that is labor-intensive, difficult to scale, and not fully reliable.

The Hebrew University study, led by Doron Zaada and Prof. Philippos Papathanos of the Department of Entomology, introduces a genetically engineered approach that produces dark-colored males and pale, yellow females. The visible difference allows for rapid and accurate sex separation, a critical step in control strategies that depend on releasing only male mosquitoes into the environment.

The study, published in the peer-reviewed Nature Communications, focuses on the Asian tiger mosquito, Aedes albopictus, an invasive species and a major disease vector worldwide. Using CRISPR gene editing, the researchers disrupted the mosquito’s yellow pigmentation gene, producing albino-like insects. They then restored normal dark pigmentation only in males by linking the pigmentation gene to nix, a key genetic factor that acts as a master switch in male sex determination.

“This produces an engineered sex-linked trait in mosquitoes that uses the insect’s own genes,” Papathanos said. “By understanding and controlling the sex determination pathway, we were able to create a system where males and females are visually different at the genetic level.”

The result is what scientists call a Genetic Sexing Strain, or GSS, in which all males are dark and all females remain pale. Because the difference is visible to the naked eye, the system allows for automated sorting without the need for complex or expensive equipment, making it more suitable for large-scale use.

Beyond simplifying sex separation, the researchers identified an additional safety feature built into the engineered strain. They found that the eggs laid by the yellow females are highly sensitive to desiccation. Unlike wild mosquito eggs, which can survive dry conditions for months, these eggs die quickly if they dry out.

“This acts as a built-in genetic containment mechanism,” Zaada said. “Even if some females are accidentally released, their eggs won’t survive in the wild, preventing any engineered strain containing our system from establishing itself in the environment.”

The study also examined whether genetically converted males retained normal behavior and reproductive capacity. According to the researchers, the engineered males closely resembled natural males in gene expression and mating behavior, suggesting that the approach does not compromise male fitness, a key requirement for successful control programs.

“Our approach provides a versatile platform for mosquito sex separation,” Papathanos noted. “By combining cutting-edge gene editing with classical genetics, we have created a scalable, safe, and efficient system.”

The gene-editing method has practical applications in mosquito control programs that rely on releasing only male mosquitoes. Techniques such as the Sterile Insect Technique require accurate sex separation to avoid releasing biting, disease-transmitting females. By making males and females visually distinct at the genetic level, the system enables fast, automated sorting and improves the reliability of population-suppression efforts.

The approach also simplifies mass rearing and supports industrial-scale mosquito production. Unlike existing methods that are labor-intensive and difficult to scale, visible genetic markers can be identified with simple optical tools, reducing costs. A built-in safety feature, in which engineered females’ eggs die if they dry out, further limits environmental risk and addresses regulatory concerns.

Beyond sterilization-based programs, the platform can be combined with other control strategies, including the release of males carrying Wolbachia bacteria or similar traits. It also allows for future customization, such as making females sensitive to heat or rearing conditions.

By Pesach Benson • December 15, 2025

Jerusalem, 15 December, 2025 (TPS-IL) — A new study has identified a specific, measurable pattern of brain activity in children with attention-deficit/hyperactivity disorder that not only distinguishes them reliably from their typically developing peers but also appears to be modifiable through a targeted, non-pharmacological intervention.

ADHD — one of the most common neurodevelopmental disorders in children, affecting an estimated 5–10 percent of children worldwide, with symptoms often continuing into adolescence and adulthood for many individuals — is characterized by persistent patterns of inattention, hyperactivity, and impulsivity that interfere with daily functioning.

The research focuses on a form of EEG signal known as aperiodic brain activity, a background neural pattern linked to the brain’s excitation–inhibition balance and overall neural efficiency. Unlike commonly used EEG markers in ADHD research, which have produced inconsistent and sometimes contradictory results, this signal consistently differentiated children with ADHD from those without the disorder in the study.

Crucially, the researchers found that this brain activity pattern is not static. In a randomized, sham-controlled trial, a subgroup of children with ADHD showed a shift toward a more typical neural profile following an intervention combining cognitive training with non-invasive brain stimulation. Some of these neural changes persisted for weeks after the treatment ended, suggesting an alteration in underlying brain dynamics rather than a short-term effect.

“ADHD is highly heterogeneous, and many of the neural markers we’ve relied on until now don’t consistently capture that complexity,” the researchers said. “Aperiodic brain activity may provide a more sensitive and reliable window into how the ADHD brain functions.”

The study was led by Dr. Ornella Dakwar-Kawar, Prof. Mor Nahum, and Prof. Itai Berger of the Hebrew University of Jerusalem, in collaboration with researchers from the University of California San Diego, the University of Surrey, partners in India, and industry. The findings were published in the peer-reviewed journal NeuroImage: Clinical.

The research followed children aged six to 12, measuring brain activity while they performed tasks requiring attention and impulse control. Children with ADHD showed elevated aperiodic EEG activity, a pattern associated with reduced neural efficiency and altered excitation–inhibition balance in the brain.

In the intervention phase, children with ADHD underwent ten sessions combining cognitive training with transcranial random noise stimulation, a painless technique that delivers mild electrical currents to targeted brain regions involved in attention and self-regulation. Children who received active stimulation showed both improved task performance and a measurable reduction in the atypical brain signal compared with those who received sham stimulation.

“This is not just about improving behavior in the moment,” the researchers said. “We’re observing changes in underlying brain dynamics that appear to move closer to typical developmental patterns.”

The findings matter because ADHD is currently diagnosed and monitored primarily through behavioral observations and reports, which can be subjective and vary across settings. While the study is preliminary, it suggests the possibility of moving beyond behavioral observations to understand the underlying brain mechanisms that drive ADHD.

One immediate application lies in the assessment of ADHD. Currently, diagnosis relies heavily on reports from parents, teachers, and clinicians, which can sometimes be inconsistent. A robust neural marker, such as the aperiodic EEG activity, could serve as a more objective measure of ADHD. Clinicians could use it to confirm diagnoses, assess symptom severity, and better distinguish ADHD from other conditions with overlapping behaviors.

Beyond diagnosis, the study suggests promising possibilities for personalized interventions and treatment monitoring. Non-pharmacological approaches, such as cognitive training combined with transcranial random noise stimulation, were shown to modify atypical brain activity in children with ADHD. Importantly, some of these changes persisted weeks after the intervention, suggesting lasting effects on neural function. In practice, this could allow clinicians to tailor interventions based on a child’s specific brain patterns and track whether treatments are producing durable changes in neural dynamics, potentially complementing or even reducing reliance on medication.

“Medication is not the only path,” the researchers said. “Targeted brain-based interventions may help rebalance neural activity in ways we can now measure objectively.”

By Pesach Benson • December 14, 2025

Jerusalem, 14 December, 2025 (TPS-IL) — Israeli and Dutch researchers have unveiled a new technique that allows scientists to precisely measure toxic protein clumps associated with Alzheimer’s disease — something that has long been out of reach and could open new paths for studying and eventually diagnosing dementia.

The technology, known as FibrilPaint combined with the FibrilRuler test, makes it possible to directly measure the length of Tau amyloid fibrils while they are still suspended in fluid, even at extremely low concentrations. Because the buildup and growth of these fibrils are closely linked to Alzheimer’s disease and related dementias, the ability to quantify their size represents a major advance for the field.

The research was led by Prof. Assaf Friedler of the Institute of Chemistry at Hebrew University of Jerusalem and Prof. Stefan G. D. Rüdiger of Utrecht University, and was published in the peer-reviewed Proceedings of the National Academy of Sciences.

Alzheimer’s disease and several other neurodegenerative disorders are marked by the abnormal accumulation of Tau proteins in the brain. Tau proteins are normal, essential proteins in the brain that help nerve cells maintain their internal structure and function. But problems arise when Tau changes shape and begins to clump abnormally. Over time, these proteins misfold and assemble into elongated amyloid fibrils, structures believed to track with disease progression. Despite their importance, scientists have struggled to measure fibril length directly in solution under realistic biological conditions.

“The length of Tau fibrils is not just a detail — it is a key parameter of the disease process,” Friedler said. “Until now, it has been extremely difficult to measure fibril size directly in solution, especially at the tiny concentrations found in real biological samples.”

Most existing techniques rely on microscopy or bulk biochemical methods that require large amounts of material, remove fibrils from their natural environment, or provide only indirect estimates of size. These limitations have made it difficult to observe how fibrils grow, fragment, or respond to potential drugs and biological pathways.

At the heart of the new approach is FibrilPaint1, a short, 22–amino acid peptide engineered to act as a highly selective fluorescent probe. Unlike conventional dyes, FibrilPaint1 binds tightly to amyloid fibrils while ignoring individual Tau molecules that have not yet aggregated, allowing researchers to distinguish harmful structures from harmless proteins in complex samples.

“We wanted a probe that behaves like a smart key,” Rüdiger said. “It finds amyloid fibrils, including very early ones, and ignores the rest of the crowded biological environment. FibrilPaint1 does exactly that.”

The probe recognizes a broad range of Tau fibrils, including those derived from patients with Alzheimer’s disease, corticobasal degeneration, and frontotemporal dementia. It also binds fibrils formed by other disease-related amyloid proteins, such as Amyloid-β, α-synuclein, and huntingtin, while showing negligible background binding to blood serum, cell lysate, or non-amyloid aggregates.

To transform this selective probe into a quantitative measuring tool, the researchers combined it with a microfluidics technique known as flow-induced dispersion analysis. In the FibrilRuler test, FibrilPaint1 binds to fibrils in solution, and the sample flows through a microscopic capillary. The way the fluorescent signal spreads during flow reveals the effective size of the fibril–probe complex, allowing researchers to calculate fibril length directly.

“This is essentially a molecular ruler that works inside the fluid itself,” Friedler said. “We no longer need to immobilize fibrils on a surface or rely on large amounts of material. We can quantify fibril length directly in solution.”

Using submicroliter sample volumes, the team measured Tau fibrils ranging from as few as four molecular layers to more than 1,100 layers, even at nanomolar concentrations. The researchers said this level of sensitivity and resolution had not previously been achievable for amyloid fibrils in solution.

The new technique has immediate value for basic research into Alzheimer’s disease and related dementias. By allowing scientists to directly measure the length of Tau fibrils in solution, at very low concentrations and in complex biological mixtures, the method makes it possible to closely track how these toxic protein structures form, grow, and break apart over time. Researchers can now study the earliest stages of fibril development, compare fibrils from different diseases or patient samples, and observe how environmental conditions influence fibril behavior, all under conditions that more closely reflect what happens in the body.

Beyond basic research, the approach could also accelerate drug development and inform future diagnostics.

And in the longer term, “if we can directly measure amyloid fibril size in patient material, such as cerebrospinal fluid, we may gain a new type of biomarker for dementia,” Rüdiger said.

Friedler stressed that clinical use would require further development and validation.

By Pesach Benson • December 2, 2025

Jerusalem, 2 December, 2025 (TPS-IL) — Israeli scientists have developed a gas sensor that can distinguish “mirror image” molecules in the air, a breakthrough with the potential to revolutionize medical diagnostics, food and beverage quality control, environmental monitoring, and pharmaceuticals, Hebrew University of Jerusalem announced.

By detecting subtle structural differences in volatile compounds, the sensors could power non-invasive breath tests for diseases such as lung cancer or diabetes, track changes in illness over time, and ensure consistency in flavor and aroma in food and fragrances. They could also help identify spoilage or contamination before products reach consumers.

Mirror-image molecules, also called chiral molecules, are pairs of molecules that have the same chemical formula but are arranged like left and right hands — identical in composition but not superimposable on each other. Even though they look nearly identical, the two forms can have very different effects, such as producing distinct smells, tastes, or biological responses.

The study, detailing the design, testing, and potential applications of the sensors, was published in the peer-reviewed journal Chem. Eur. J.

The sensor uses carbon nanotubes coated with specially designed sugar-based receptors, which act like a molecular lock-and-key to interact with specific airborne chemicals. “By adding a sugar coating, we created a precise chemical architecture around the sensor that can even interact with very weakly binding scent molecules,” said Prof. Shlomo Yitzchaik, one of the study’s supervisors.

The research team, led by Ariel Shitrit and Yonatan Sukhran under the guidance of Yitzchaik and Prof. Mattan Hurevich, demonstrated that the sensors could clearly differentiate between mirror-image forms of limonene and carvone, two common scent molecules, while showing no reaction to similar forms of α-pinene. Remarkably, the sensors detected the (–)-limonene molecule at concentrations as low as 1.5 parts per million, roughly ten times more sensitive than many comparable methods.

The sensors’ effectiveness comes from the interaction between the sugar-coated nanotubes and the airborne molecules. Using electrical measurements combined with computer simulations in collaboration with Germany’s Technical University of Dresden and Friedrich Schiller University Jena, the researchers found that each molecular mirror image binds slightly differently to the receptor. These tiny differences alter electron movement in the nanotubes, producing measurable changes in the electrical signal.

“Understanding how molecular structure affects sensor performance gives us a blueprint for designing better artificial smell receptors,” said Hurevich. By testing different receptor designs, the team identified chemical features that improve selectivity, paving the way for more precise and versatile sensors.

The research is part of the European SMELLODI consortium, which explores links between body odor, smell perception, and physiological and emotional states. Non-invasive analysis of volatile organic compounds—including mirror-image molecules—is a key goal of the project, with potential applications in health monitoring, environmental safety, and industry.

Transforming sugar molecules, which normally dissolve in water, into stable, functional gas sensors posed a significant chemical and engineering challenge. The team overcame this by creating a two-part system: adjustable sugar-based receptors chemically attached to carbon nanomaterials. The design can be fine-tuned by altering the sugar “frame” or the chemical groups attached to it, enabling tailored detection capabilities.

Beyond healthcare and food, the sensors could have applications in environmental monitoring and pharmaceuticals. They can detect air pollutants or chemical leaks at extremely low levels, improving safety for both people and ecosystems. In drug manufacturing and chemical research, the sensors could verify the purity and composition of chiral molecules, which often have different biological effects depending on their mirror-image form, helping ensure products are safe and effective.

Looking ahead, the researchers believe computational tools, including advanced physics simulations and machine learning, could accelerate the creation of new receptor designs, expanding the range of detectable airborne molecules and their mirror-image forms.

“Our work shows that tiny changes in molecular structure can be picked up reliably using sugar-coated nanotubes,” Shitrit said. “This opens the door to electronic sensing systems that were previously thought impossible.”