The surprising study was led by Dr. Natalia Kononov, who completed her doctorate under the supervision of Prof. Danit Ein-Gar at the Coller School of Management at Tel Aviv University and is now a postdoctoral fellow at the Wharton School of Business at the University of Pennsylvania. The study, conducted in collaboration with Prof. Ein-Gar and Prof. Stefano Puntoni of Wharton, was published in the International Journal of Research in Marketing.

Prof. Danit Ein-Gar (Photo credit: Israel Hadari).

“When we enhance our appearance and feel beautiful—for example, after a fresh haircut—we behave in a more socially conscious manner”, explains Prof. Ein-Gar. “Why? Because we feel as though all eyes are on us, drawing attention, and so we strive to act better. It’s easy to criticize the selfie generation, constantly beautifying themselves and sharing polished photos, but we demonstrate a side effect of this behavior that can benefit society. People who feel good about their appearance can channel that feeling into good deeds”.

Dr. Natalia Kononov.

To test their hypothesis, the researchers conducted a series of experiments, some in virtual settings and others in a laboratory. In one lab experiment, participants were asked to use a filter to enhance a selfie they had taken. A control group, meanwhile, was asked to enhance a photo of an object in the room.

“The experimental group consisted of 50 participants, as did the control group”, Prof. Ein-Gar explains. “After viewing their enhanced photo, each participant collected an envelope with their payment in cash. Next to the payment envelope, there was a donation box so participants could voluntarily donate some or all of their payment. We observed that members of the experimental group, who saw themselves as more attractive, donated up to twice as much as those in the control group. It’s enough to imagine ourselves as more attractive—even just envisioning a more polished digital version of ourselves—to encourage prosocial behavior. This insight has significant practical implications. Until now, research has focused on the appearance of the donation seekers—whether the recipient or the fundraiser—and indeed, more attractive fundraisers have been found to raise more money. Our study introduces another relevant factor: the donor’s appearance. This opens the door to innovative strategies for streamlining charity campaigns, such as partnering with cosmetic companies, hairdressers, and beauty salons—for everyone’s benefit”.

Beauty and the Benefit

One of the most surprising experiments was conducted virtually, on Facebook. Clicking on a link randomly directed users to one of two “know yourself” questionnaires. The control group’s questionnaire asked about preferred architectural styles, while the experimental group’s questionnaire included questions about fashion styles and was designed to make respondents imagine themselves at their most attractive moments, such as envisioning themselves dressed up for a fancy social event. At the end of the questionnaire, a seemingly unrelated pop-up appeared with a link to a donation page. About 7% of respondents who answered the “beauty” questionnaire clicked on the donation link, compared to approximately 2% of those who answered the architectural questionnaire—a particularly impressive figure considering the average click-through rate on Facebook links is just 0.9%.

“Our society is obsessively focused on physical appearance while simultaneously criticizing this superficial behavior”, says Dr. Kononov. “People who are appearance-focused are often judged harshly, but we show that this behavior can have positive spillover effects that benefit others. Social mechanisms may evolve to create some balance, where behaviors that serve the individual are accompanied by byproducts that contribute to the greater good“.

The study was led by the lab of Prof. Boaz Barak and PhD student Inbar Fischer from the Sagol School of Neuroscience and the School of Psychological Sciences at Tel Aviv University, in collaboration with the labs of Prof. Ben Maoz from the Department of Biomedical Engineering at Fleischman Faculty of Engineering at Tel Aviv University and Prof. Shani Stern from the Department of Neurobiology at the University of Haifa. The article was published in the prestigious journal Science Advances.

PhD student Inbar Fischer.

Prof. Barak: "Autism is a relatively common neurodevelopmental disorder. According to current data, 1-2% of the global population and one in every 36 boys in the U.S. are diagnosed with autism spectrum disorder (ASD), with numbers rising over time. Autism is caused by a wide range of factors - environmental, genetic, and even social and cultural (such as the rise in parental age at conception). In my lab, we study the genetic causes of autism. Among these are mutations in a gene called SHANK3. The impact of these mutations on the function of brain neurons has been extensively studied, and we know that the protein encoded by SHANK3 plays a central role in binding receptors in the neuron, essential for receiving chemical signals (neurotransmitters and others) by which neurons communicate. Thus, damage to this gene can disrupt message transmission between neurons, impairing the brain's development and function. In this study we sought to shed light on other, previously unknown mechanisms, through which mutations in the SHANK3 gene disrupt brain development, leading to disorders manifested as autism".

Specifically, the research team focused on two components in the brain that have not yet been studied extensively in this context: non-neuronal brain cells (glia) called oligodendrocytes and the myelin they produce. Myelin tissue is a fatty layer that insulates nerve fibers (axons), similar to the insulating layer that coats electrical cables. When the myelin is faulty, the electrical signals transmitted through the axons may leak, disrupting the message transmission between brain regions and impairing brain function.

How a Gene Mutation Impacts the Brain

The team employed a genetically engineered mouse model for autism, introducing a mutation in the Shank3 gene that mirrors the mutation found in humans with this form of autism. Inbar Fischer: "Through this model, we found that the mutation causes a dual impairment in the brain's development and proper function: first, in oligodendrocytes, as in neurons, the SHANK3 protein is essential for the binding and functioning of receptors that receive chemical signals (neurotransmitters and others) from neighboring cells. This means that the defective protein associated with autism disrupts message transmission to these vital support cells. Secondly, when the function and development of oligodendrocytes is impaired, their myelin production is also disrupted. The faulty myelin does not properly insulate the neuron’s axons, thereby reducing the efficiency of electrical signal transmission between brain cells, as well as the synchronization of electrical activity between different parts of the brain. In our model, we found myelin impairment in multiple brain areas and observed that the animals' behavior was adversely affected as a result".

The researchers then sought a method for fixing the damage caused by the mutation, with the hope of ultimately developing a treatment for humans. Inbar Fischer: "We obtained oligodendrocytes from the brain of a mouse with a Shank3 mutation, and inserted DNA segments containing the normal human SHANK3 sequence. Our goal was to allow the normal gene to encode a functional and normal protein, which, replacing the defective protein, would perform its essential role in the cell. To our delight, following treatment, the cells expressed the normal SHANK3 protein, enabling the construction of a functional protein substrate to bind the receptors that receive electrical signals. In other words, the genetic treatment we had developed repaired the oligodendrocytes' communication sites, essential for the cells’ proper development and function as myelin producers".

To validate findings from the mouse model, the research team generated induced pluripotent stem cells from the skin cells of a girl with autism caused by a SHANK3 gene mutation identical to that in the mice. From these stem cells, they derived human oligodendrocytes with the same genetic profile. These oligodendrocytes displayed impairments similar to those observed in their mouse counterparts.

Autism and Myelin Damage: New Hope for Treatment

Prof. Barak concludes: "In our study, we discovered two new brain mechanisms involved in genetically induced autism: damage to oligodendrocytes and, consequently, damage to the myelin they produce. These findings have important implications – both clinical and scientific.  Scientifically, we learned that defective myelin plays a significant role in autism and identified the mechanism causing the damage to myelin. Additionally, we revealed a new role for the SHANK3 protein: building and maintaining a functional binding substrate for receptors critical for message reception in oligodendrocytes (not just in neurons). We discovered that contrary to the prevailing view, these cells play essential roles in their own right, far beyond the support they provide for neurons — often seen as the main players in the brain. In the clinical sphere, we validated a gene therapy approach that led to significantly improved development and function of oligodendrocytes derived from the brains of mice modeling autism. This finding offers hope for developing genetic treatment for humans, which could improve the myelin production process in the brain. Furthermore, recognizing the significance of myelin impairment in autism—whether linked to the SHANK3 gene or not—opens new pathways for understanding the brain mechanisms underlying autism and paves the way for future treatment development".

The study was led by Dr. Antonella Ruggiero, Leore Heim, and Dr. Lee Susman from Prof. Inna Slutsky’s lab at the Faculty of Medical and Health Sciences at Tel Aviv University. Prof. Slutsky, who is also affiliated with the Sagol School of Neuroscience, heads the Israeli Society for Neuroscience and directs the Sieratzki Institute for Advances in Neuroscience. Additional researchers included Dr. Ilana Shapira, Dima Hreaky, and Maxim Katsenelson from the Faculty of Medical and Health Sciences at Tel Aviv University, and Prof. Kobi Rosenblum from the University of Haifa. The study was published in the prestigious journal Neuron.

“In recent decades, brain research has mainly focused on processes that allow information encoding, memory, and learning, based on changes in synaptic connections between nerve cells”, says Prof. Slutsky.

“But the brain’s fundamental stability, or homeostasis, is essential to support these processes. In our lab, we explore the mechanisms that maintain this stability, and in this study, we focused on the NMDAR—a receptor known to play a role in learning and memory”, Slutsky continues.

This comprehensive project used three primary research methods: electrophysiological recordings from neurons in both cultured cells (in vitro) and living, behaving mice (in vivo) within the hippocampus, combined with computational modeling (in silico). Each approach provided unique insights into how NMDARs contribute to stability in neural networks.

Dr. Antonella Ruggiero studied NMDAR function in cultured neurons using an innovative technique called “dual perturbation”, developed in Prof. Slutsky’s lab. “First, I exposed neurons to ketamine, a known NMDAR blocker”, she explains. “Typically, neuronal networks recover on their own after disruptions, with activity levels gradually returning to baseline due to active compensatory mechanisms. But when the NMDAR was blocked, activity levels stayed low and didn’t recover. Then, with the NMDAR still blocked, I introduced a second perturbation by blocking another receptor. This time, the activity dropped and recovered as expected, but to a new, lower baseline set by ketamine, not the original level”. This finding reveals the NMDAR as a critical factor in setting and maintaining the activity baseline in neuronal networks. It suggests that NMDAR blockers may impact behavior not only through synaptic plasticity but also by altering homeostatic set points.

Building on this discovery, Dr. Ruggiero sought to uncover the molecular mechanisms behind the NMDAR’s role in tuning the set point. She identified that NMDAR activity enables calcium ions to activate a signaling pathway called eEF2K-BDNF, previously linked to ketamine’s antidepressant effects.

How NMDARs Set the Brain’s Activity Baseline

Leore Heim investigated whether the NMDAR similarly affects baseline activity in the hippocampus of living animals. A major technical challenge was administering an NMDAR blocker directly to the hippocampus without affecting other brain areas, while recording long-term activity at the individual neuron level. “Previous studies often used injections that delivered NMDAR blockers across the entire brain, leading to variable and sometimes contradictory findings,” he explains. “To address this, I developed a method combining direct drug infusion into the hippocampus with long-term neural activity recording in the same region. This technique revealed a consistent decrease in hippocampal activity across states like wakefulness and sleep, with no compensatory recovery as seen with other drugs. This strongly supports that NMDARs set the activity baseline in hippocampal networks in living animals”.

Mathematician Dr. Lee Susman created computational models to answer a longstanding question: Is brain stability maintained at the level of the entire neural network, or does each neuron individually stabilize itself? “Based on the data from Antonella and Leore’s experiments, I found that stability is maintained at the network level, not within single neurons,” he explains. “Using models of neural networks, I showed that averaging activity across many neurons provides computational benefits, including noise reduction and enhanced signal propagation. However, we need to better understand the functional significance of single-neuron drift in future studies”.

Prof. Slutsky adds: “We know that ketamine blocks NMDARs, and in 2008, it was FDA-approved as a rapid-acting treatment for depression. Unlike typical antidepressants like Cipralex and Prozac, ketamine acts immediately by blocking NMDARs. However, until now, it wasn’t fully understood how the drug produced its antidepressant effects. Our findings suggest that ketamine’s actions may stem from this newly discovered role of NMDAR: reducing the activity baseline in overactive brain regions seen in depression, like the lateral habenula, without interfering with homeostatic processes. This discovery could reshape our understanding of depression and pave the way for developing innovative treatments".

A new study from the School of Zoology  and the Steinhardt Museum of Natural History  at Tel Aviv University has revealed that the Oriental hornet is the only known animal capable of chronically consuming alcohol in high concentrations with almost no negative effects on its health or lifespan. The research team says, "This is a remarkable animal that shows no signs of intoxication or illness even after ingesting huge amounts of alcohol."

The research was conducted under the leadership of postdoctoral fellow Dr. Sofia Bouchebti from Prof. Eran Levin's laboratory at Tel Aviv University’s School of Zoology and the Steinhardt Museum of Natural History. The study was published in the journal Proceedings of the National Academy of Sciences of the United States of America (PNAS).

The researchers explain that alcohol is commonly produced in nature through the breakdown of sugars by yeasts and bacteria, primarily found in ripe fruits and nectar. Although alcohol contains nearly twice the amount of energy as sugar, it is toxic to most animals — including us humans — with occasional consumption, and especially with chronic use. Among the animals known to consume alcohol are fruit flies, which show signs of alcohol poisoning even at relatively low concentrations, and treeshrews — mammals native to East Asia that feed on ripe, alcohol-rich fruits — who show symptoms such as fatty liver and other effects indicative of alcoholism after consuming low concentrations of alcohol continuously for several days.

As for humans, many of us like consuming alcohol. Humans domesticated the wine grape around 10,000 years ago, and compared to other animals, we can tolerate and often enjoy consuming relatively high amounts of alcohol. However, as we know, alcohol has significant effects on behavior, cognition, and, of course, health, with a host of diseases linked to its consumption.

Hornets Can Handle Their Liquor

In the new study, the research team tested the Oriental hornet’s ability to consume alcohol and break it down. Dr. Bouchebti explains: "The hornets naturally store yeasts in their digestive system, which provides them with a unique environment that allows the yeast to develop and reproduce, creating new strains. One explanation is that hornets transfer yeasts to fruits, which indirectly contributes to the production of wine. In our study, we labeled the alcohol consumed by the hornets with a heavy carbon isotope. As the alcohol is metabolized, it breaks down into carbon dioxide, which is exhaled. By measuring the amount of labeled carbon dioxide emitted, we were able to estimate the speed at which the alcohol was broken down. The findings were surprising; we were amazed to see the rapid rate at which the hornets metabolized the alcohol".

In the next stage, the researchers sought to determine whether the Oriental hornet ever becomes intoxicated. Does increased alcohol consumption affect their behavior, for example causing aggression or impacting their nest-building abilities? Here too, the findings were surprising: even when consuming high concentrations of alcohol (80 percent alcohol as the sole source of nutrition) there was no noticeable effect on the hornets’ behavior. In the final phase of the study, the researchers tested whether alcohol had any impact on the hornets’ lifespan and health. Once again, they were amazed to discover that no differences were found between the lifespan of hornets that consumed only alcohol for their entire lives (three months) and hornets that consumed sugar water.

No Hangovers Here

Prof. Levin concludes: "To the best of our knowledge, Oriental hornets are the only animal adapted to consuming alcohol as a metabolic fuel. They show no signs of intoxication or illness, even after chronically consuming huge amounts of alcohol, and they eliminate it from their bodies very quickly. In a bioinformatics analysis of the Oriental hornet’s genome, conducted by Prof. Dorothee Huchon, it was discovered that the hornet possesses several copies of the gene responsible for producing the enzyme that breaks down alcohol; this genetic adaptation may be related to their incredible ability to handle alcohol. We propose that the ancient relationship between hornets and yeast led to the development of this adaptation. Furthermore, while alcohol-related research is highly advanced, with 5.3 percent of deaths in the world linked to alcohol consumption, we believe that, following our research, Oriental hornets could potentially be used to develop new models for studying alcoholism and the metabolism of alcohol".