The Fondation Weizmann.be pour la science is a non-profit, private entity. Its aim is to promote the Weizmann Institute of Science in Belgium and to support its research projects via appropriate public relations activities as well as selective fund raising, in particular in the form of sponsorships, donations and legacies.
One of the Foundation’s regular activites is the sponsoring of promising students attending Belgian secondary schools, who qualify for participation in the annual 4 weeks International Scientific Summer School (ISSI) on the Weizmann Institute of Science campus, before continuing their tertiary education in science. This year two promising young women have been selected.
The Foundation is chaired by Mr Christian Hendboeg.
Mrs Diane Culer, Prof. Pierre Klees, Prof Maurice Sosnowski, Mr Paul de Schietere de Lophem, Mr Eric Hemeleers and Mr Roland Louis are directors.
The Belgian Foundation was founded in 2006, replacing the Belgian Committee, which had been established in 1973 by Prof. Georges Schnek, who also served as the first Secretary General until 1979. He was succeeded by Mr Louis Culer, who held this position for 20 years until 1999, followed by Prof. Marc van Montagu until June 2006.
Among the former Chairmen of the Committee were the former Belgian Prime Minister Theo Lefèvre (1973-1975), Prof. Piet de Somer, Rector of the “Katolieke Universiteit Leuven” (1975-1980) and Prof. Jean Brachet (1980-1972). Two Nobel Laureates, Prof. Christian de Duve and Prof. Ilya Prigogine, were members of the Academic Council.
A bacterial model helps reveal how our bodies prevent population explosions – and cancer
It follows that a balance between dividing and mature cells is a precondition for the existence of any multicellular organism, but how is it maintained? In a new study published recently in Cell, researchers from the Weizmann Institute of Science used single-celled organisms to better understand how multicellular organisms maintain this equilibrium and protect themselves from cancer.
Cell differentiation is a biological “specialization training,” in which a stem cell divides into two daughter cells, one of which assumes a defined role and acquires the characteristics needed to fulfill it. When cells undergo differentiation, their new specialty is useful to the multicellular organism of which they are a part, but they pay a heavy individual toll: The further they get along this specialization pathway, the more their ability to replicate decreases, until they are no longer able to divide at all. This slow division of differentiated cells makes them vulnerable to populations of cells that divide and grow at a faster rate and can therefore take over the tissue and its resources. In some types of blood cancer, for example, stem cells in the bone marrow undergo a mutation that slows their differentiation and allows them to produce more daughter stem cells. These mutant cells take advantage of the natural weak point in the differentiation process, overcoming the population of healthy cells in a process known as mutant takeover.
“To determine which differentiation rate works best, we held a competition between 11 strains of E. coli, each of which cuts out DNA segments – that is, differentiates – at a different rate”
Even though one mutation, on average, occurs in every cell division in our bodies, most of us enjoy decades of good health, through countless cell divisions, without experiencing mutant takeover. This suggests that there are effective mechanisms for dealing with this threat, even if they are hard to identify in complex organisms. Scientists in Prof. Uri Alon’s research group at Weizmann’s Molecular Cell Biology Department decided to engineer E. coli bacteria, which do not usually differentiate, so as to make them undergo an artificial differentiation process, allowing researchers to study how a cell population deals with mutant takeover.
“There are a number of clear advantages to the E. coli model,” explains Dr. David Glass, who led the study in Alon’s lab. “One of them is a short generation time, which allowed us to study the development of mutants over hundreds of generations in the lab.” In order to produce E. coli bacteria capable of differentiating, researchers took inspiration from cyanobacteria called Anabaena, which differentiate – by cutting out certain segments of their DNA – in response to a shortage of nitrogen in their environment. Although the differentiated bacteria lose the ability to divide, they gain an important survival edge: the ability to supply themselves and the entire colony with nitrogen.
To mimic the differentiation process in the E. coli model, the scientists grew the bacteria in an environment that included antibiotics but lacked an essential amino acid. Using genetic engineering, they inserted into each bacterium several copies of a gene for resistance to antibiotics and several copies of a gene that produced the missing amino acid. Before the process of artificial differentiation began – that is, when the bacteria were in a state equivalent to that of stem cells – the antibiotic-resistance genes were active, so the bacteria were able to divide and differentiate at a high rate despite the presence of the antibiotic. When the differentiation process started by means of cutting out the antibiotic resistance genes, the bacteria gradually lost their ability to divide and differentiate, but they gained a survival advantage: The cuts in the DNA gradually activated the genes that produced the essential amino acid.
“To determine which differentiation rate works best, we held a competition between 11 strains of E. coli, each of which cuts out DNA segments – that is, differentiates – at a different rate,” Glass explains. “We mixed equal quantities of the bacteria, grew them over the course of a few days and then checked to see which had survived. We discovered a very strong selection in favor of bacteria that differentiated at a moderate rate and found that strains of bacteria with a moderate rate of differentiation maintained the optimal balance of cell types in their population. At any given moment, only a minority of the cells were ‘pure stem cells’ or ‘fully differentiated cells,’ and a majority were found in intermediate states of the process.”
This optimal, moderate differentiation rate is shared by various systems in the human body, in which a quantitative balance is maintained among stem cells, progenitor cells at different stages of differentiation and differentiated cells that occasionally die and are replaced by new ones.
To keep the population size steady, it is important to maintain that equilibrium even when environmental conditions change. To find out whether the bacteria in their model indeed maintained this equilibrium even under changed conditions, the researchers grew them in 36 different combinations of antibiotic and amino acid concentrations in the culture medium. “We saw that in every situation – apart from the most extreme ones, such as a total absence of antibiotics – the cells’ optimal differentiation rate remained in the moderate range and the equilibrium was maintained,” Glass explains. “This means that the population equilibrium characterizing the differentiation model we developed is, to a large extent, immune to environmental changes and threats.” But is a population of bacteria that is differentiating at an optimal rate also immune to mutant takeover, like the systems in multicellular organisms?
To test the ability of these bacteria to withstand mutant takeover, the researchers grew them over many generations and checked whether random mutations appeared during the long growth period, creating bacteria that do not differentiate at all and divide uncontrollably. In other words, do mutant bacteria bring about mutant takeover, or are they suppressed at an early stage? The first time they conducted the experiment, the researchers were disappointed to find mutant takeovers in half of the cases. “We found that when a genetic change breaks the connection between differentiation slowdown and getting that survival advantage, mutants that do not differentiate can take over,” Glass adds.
“Many diseases are unique to multicellular organisms. When we genetically engineer more and more characteristics of multicellular systems in single-celled organisms, we can uncover the weak points”
Next the researchers repeated the experiment with a new bacterial strain that was genetically engineered to be immune to the identified mutation. “We managed to grow around 270 generations of differentiating bacteria, and no mutant takeover occurred. Unfortunately, the invasion of Israel on October 7 cut the experiment short, and the bacteria may well be even more resilient,” Glass says. “We showed that a system in which differentiating E. coli cells stop dividing but gain a survival advantage can maintain an optimal population balance and avert mutant takeover. Many diseases, such as cancer and autoimmune disorders, are unique to multicellular organisms. When we genetically engineer more and more characteristics of multicellular systems in single-celled organisms, we can uncover the weak points and look for them in human tissue too.”
“Beyond basic science, these new findings could also have an impact on the use of bacteria in industry,” Glass adds. “Genetically engineered bacteria are currently used in the large-scale production of insulin, enzymes and other substances used by humans. Creating a population of differentiating bacteria that maintains its equilibrium, renews itself and even prevents mutant takeover could be very useful in these production processes.”
Study participants included Dr. Anat Bren, Elizabeth Vaisbourd and Dr. Avi Mayo from Weizmann’s Molecular Cell Biology Department.
Researchers from the University of Michigan and the Weizmann Institute develop the first-ever complete central nervous system on a chip: It faithfully emulates that of a human embryo, from the forebrain to the bottom of the spinal cord
Once upon a time, we were all nothing but a mass of densely packed stem cells. Over time, this mass elongated, sprouted limbs on either side, buttocks at the rear, a stomach in the front and a head on the top. The process by which embryonic stem cells give rise to distinct organs, rescuing us from an amorphous fate, occurs thanks to morphogens, molecules that are manufactured at specific times and places within the embryo and dispersed to dictate the location and shape of our organs. The varying concentrations of morphogens serve as a map that guides the stem cells to their destination and destiny.
Morphogen concentration maps are key to all technologies aimed at making organoids, the laboratory-manufactured miniature versions of living organs that in the past decade have taken over the world of developmental biology. But until now, most researchers have been producing organoids using uniform concentrations of morphogens in petri dishes, which limited them to growing small sections of an organ in each dish, rather than generating a single, miniature version of the complete organ. Now, however, researchers from the University of Michigan, who were led by Prof. Jianping Fu and Dr. Xufeng Xue, from the Weizmann Institute of Science and from the University of Pennsylvania have created a miniature version of the entire embryonic central nervous system, from the brain to the bottom of the spinal cord, using a microfluidic chip that mimics the dispersal of the morphogens during embryonic development.
The new chip will enable researchers to ask entirely new questions, both about the development of a healthy embryo and about diseases and tissue damage, according to study participant Prof. Orly Reiner of Weizmann’s Molecular Genetics Department. She has been studying diseases affecting the developing brain for more than 30 years and started growing organoids in her laboratory about a decade ago. “Organoids were already exposed to varying concentrations of morphogens in past studies, but those studies generated only small sections of the central nervous system – for example, just the spinal cord or the forebrain, but not both,” she explains.
The microfluidic chip allows researchers to pour morphogens, from almost any direction and at any time they want, into reservoirs that contain the organoids. At the center of the chip are narrow, adhesive surfaces that are 4 millimeters long, just like the central nervous system of a month-old embryo. Stem cells are embedded along the length of these surfaces, which are then covered with a gel that simulates the extracellular environment, allowing them to develop into three-dimensional tissue. Within a short period of time, the cells spontaneously organize themselves into a hollow tube. After three days, through a reservoir on one end of the chip, the researchers start adding morphogens, which diffuse slowly across the length or breadth of the tissue.
“We saw perfect order along the entire length of the central nervous system, just as it appears in the early embryonic stage”
The researchers soon saw that the stem cells on the chip matured into a variety of different cell types of the embryonic central nervous system. The side of the chip with the high concentration of morphogens gave rise to cells that developed into the end of the spinal cord, followed by the cells destined for the middle of the spinal cord, the hindbrain, the midbrain and, at the furthest extremity, the forebrain. “When we characterized the new organoids, we saw perfect order along the entire length of the central nervous system, just as it appears in the early embryonic stage,” Reiner says.
Having created the central nervous system’s longitudinal tube, the researchers took on another challenge: to emulate the development of the embryo’s forebrain along the ventral-dorsal axis. Two important cell types that are essential to the functioning of the adult brain are usually generated in the forebrain: excitatory neurons, which encourage neuronal firing, and inhibitory neurons, which block this firing. “Until now, we had to grow each of these cell types on a different plate by exposing two organoids to different morphogen concentrations, and then try to join them together,” Reiner explains.
But the new microfluidic chip enabled the researchers to distribute the concentrations of morphogens so that the two types of neurons were generated in the same tissue. To do this, they first created the longitudinal tube, as described above, and on the seventh day they poured in morphogens near the forebrain but far from the spinal cord. Within a short period of time, cells that would later turn into inhibitors appeared on the inside of the tube, while those destined to become excitatory cells appeared on the outside of the tube – exactly as happens during embryonic development.
The researchers note that their chip does not emulate the earliest stages of the central nervous system’s development. “We are actually skipping over the early stages and pushing the stem cells to the stage of development typical of a four-week-old embryo,” Reiner says. Still, within days a three-dimensional tissue formed, and it bore a remarkable resemblance to the embryo’s central nervous system, both in terms of the cells it contained and the order of their appearance. This allowed the team to study, for example, the genes involved in the differentiation of cell populations in the spinal cord, a process that was not previously understood.
The chip is already helping researchers further their understanding of issues related to the development of the human nervous system. Reiner’s team, for one, has integrated the technology into its work and is using the chip to study how genetic diseases affect the longitudinal development of parts of the brain. They hope that more researchers will use the technology to expand our understanding of a wide range of diseases that damage the nervous system.
Also participating in the study were Dr. Yung Su Kim, Dr. Norio Kobayashi, Dr. Yue Liu, Dr. Jason R. Spence, Dr. Robin Zhexuan Yan, Dr. Yu-Hwai Tsai, Shiyu Sun and Yi Zheng from the University of Michigan; Dr. Rami Yair Tshuva and Alfredo-Isaac Ponce-Arias from Weizmann’s Molecular Genetics Department; Prof. Hongjun Song, Prof. Guo-Li Ming and Dr. Richard O’Laughlin from the University of Pennsylvania; and Prof. Azim Surani and Dr. Frederick C. K. Wong from Cambridge University.
A bacterial model helps reveal how our bodies prevent population explosions – and cancer
It follows that a balance between dividing and mature cells is a precondition for the existence of any multicellular organism, but how is it maintained? In a new study published recently in Cell, researchers from the Weizmann Institute of Science used single-celled organisms to better understand how multicellular organisms maintain this equilibrium and protect themselves from cancer.
Cell differentiation is a biological “specialization training,” in which a stem cell divides into two daughter cells, one of which assumes a defined role and acquires the characteristics needed to fulfill it. When cells undergo differentiation, their new specialty is useful to the multicellular organism of which they are a part, but they pay a heavy individual toll: The further they get along this specialization pathway, the more their ability to replicate decreases, until they are no longer able to divide at all. This slow division of differentiated cells makes them vulnerable to populations of cells that divide and grow at a faster rate and can therefore take over the tissue and its resources. In some types of blood cancer, for example, stem cells in the bone marrow undergo a mutation that slows their differentiation and allows them to produce more daughter stem cells. These mutant cells take advantage of the natural weak point in the differentiation process, overcoming the population of healthy cells in a process known as mutant takeover.
“To determine which differentiation rate works best, we held a competition between 11 strains of E. coli, each of which cuts out DNA segments – that is, differentiates – at a different rate”
Even though one mutation, on average, occurs in every cell division in our bodies, most of us enjoy decades of good health, through countless cell divisions, without experiencing mutant takeover. This suggests that there are effective mechanisms for dealing with this threat, even if they are hard to identify in complex organisms. Scientists in Prof. Uri Alon’s research group at Weizmann’s Molecular Cell Biology Department decided to engineer E. coli bacteria, which do not usually differentiate, so as to make them undergo an artificial differentiation process, allowing researchers to study how a cell population deals with mutant takeover.
“There are a number of clear advantages to the E. coli model,” explains Dr. David Glass, who led the study in Alon’s lab. “One of them is a short generation time, which allowed us to study the development of mutants over hundreds of generations in the lab.” In order to produce E. coli bacteria capable of differentiating, researchers took inspiration from cyanobacteria called Anabaena, which differentiate – by cutting out certain segments of their DNA – in response to a shortage of nitrogen in their environment. Although the differentiated bacteria lose the ability to divide, they gain an important survival edge: the ability to supply themselves and the entire colony with nitrogen.
To mimic the differentiation process in the E. coli model, the scientists grew the bacteria in an environment that included antibiotics but lacked an essential amino acid. Using genetic engineering, they inserted into each bacterium several copies of a gene for resistance to antibiotics and several copies of a gene that produced the missing amino acid. Before the process of artificial differentiation began – that is, when the bacteria were in a state equivalent to that of stem cells – the antibiotic-resistance genes were active, so the bacteria were able to divide and differentiate at a high rate despite the presence of the antibiotic. When the differentiation process started by means of cutting out the antibiotic resistance genes, the bacteria gradually lost their ability to divide and differentiate, but they gained a survival advantage: The cuts in the DNA gradually activated the genes that produced the essential amino acid.
“To determine which differentiation rate works best, we held a competition between 11 strains of E. coli, each of which cuts out DNA segments – that is, differentiates – at a different rate,” Glass explains. “We mixed equal quantities of the bacteria, grew them over the course of a few days and then checked to see which had survived. We discovered a very strong selection in favor of bacteria that differentiated at a moderate rate and found that strains of bacteria with a moderate rate of differentiation maintained the optimal balance of cell types in their population. At any given moment, only a minority of the cells were ‘pure stem cells’ or ‘fully differentiated cells,’ and a majority were found in intermediate states of the process.”
This optimal, moderate differentiation rate is shared by various systems in the human body, in which a quantitative balance is maintained among stem cells, progenitor cells at different stages of differentiation and differentiated cells that occasionally die and are replaced by new ones.
To keep the population size steady, it is important to maintain that equilibrium even when environmental conditions change. To find out whether the bacteria in their model indeed maintained this equilibrium even under changed conditions, the researchers grew them in 36 different combinations of antibiotic and amino acid concentrations in the culture medium. “We saw that in every situation – apart from the most extreme ones, such as a total absence of antibiotics – the cells’ optimal differentiation rate remained in the moderate range and the equilibrium was maintained,” Glass explains. “This means that the population equilibrium characterizing the differentiation model we developed is, to a large extent, immune to environmental changes and threats.” But is a population of bacteria that is differentiating at an optimal rate also immune to mutant takeover, like the systems in multicellular organisms?
To test the ability of these bacteria to withstand mutant takeover, the researchers grew them over many generations and checked whether random mutations appeared during the long growth period, creating bacteria that do not differentiate at all and divide uncontrollably. In other words, do mutant bacteria bring about mutant takeover, or are they suppressed at an early stage? The first time they conducted the experiment, the researchers were disappointed to find mutant takeovers in half of the cases. “We found that when a genetic change breaks the connection between differentiation slowdown and getting that survival advantage, mutants that do not differentiate can take over,” Glass adds.
“Many diseases are unique to multicellular organisms. When we genetically engineer more and more characteristics of multicellular systems in single-celled organisms, we can uncover the weak points”
Next the researchers repeated the experiment with a new bacterial strain that was genetically engineered to be immune to the identified mutation. “We managed to grow around 270 generations of differentiating bacteria, and no mutant takeover occurred. Unfortunately, the invasion of Israel on October 7 cut the experiment short, and the bacteria may well be even more resilient,” Glass says. “We showed that a system in which differentiating E. coli cells stop dividing but gain a survival advantage can maintain an optimal population balance and avert mutant takeover. Many diseases, such as cancer and autoimmune disorders, are unique to multicellular organisms. When we genetically engineer more and more characteristics of multicellular systems in single-celled organisms, we can uncover the weak points and look for them in human tissue too.”
“Beyond basic science, these new findings could also have an impact on the use of bacteria in industry,” Glass adds. “Genetically engineered bacteria are currently used in the large-scale production of insulin, enzymes and other substances used by humans. Creating a population of differentiating bacteria that maintains its equilibrium, renews itself and even prevents mutant takeover could be very useful in these production processes.”
Study participants included Dr. Anat Bren, Elizabeth Vaisbourd and Dr. Avi Mayo from Weizmann’s Molecular Cell Biology Department.
Around 300,000,000,000 cells are born and die in our bodies every day – that’s about 4,000,000 every second – and 90 percent of them are blood cells.
Prof. Uri Alon is the head of the Sagol Institute for Longevity Research and the incumbent of the Abisch-Frenkel Professorial Chair. His research is also supported by the Rising Tide Foundation.
A Weizmann Institute method for tracking the effects of drugs on zebrafish may help develop improved therapies for depression and other mood-related disorders
Psychedelics are a hot topic in labs all over the world because they hold great potential for relieving the symptoms of depression, anxiety, PTSD and other mood-related conditions. Still, there is a major hurdle to developing these substances into safe, effective medications: Very little is known about how psychedelic drugs work.
In a study reported recently in Molecular Psychiatry, a team headed by Dr. Takashi Kawashima at the Weizmann Institute of Science has developed a new approach that makes it possible to observe how psychedelics influence behavior and how they affect individual cells in the brain. The method combines powerful optical microscopy, advanced image analysis and artificial intelligence, and uses immature, larval zebrafish as its animal model.
Targeting serotonin for mental health
Psychedelics have been with us for thousands of years, from ancient shamanistic rituals to today’s wild parties. They were placed off limits for scientific study by the Comprehensive Drug Abuse Prevention and Control Act of 1970, which inaugurated the United States’ “war on drugs.” Recently, however, psychedelics have made it to the right side of the law.
According to Kawashima, who in addition to being a research neuroscientist is a medical doctor, psychedelics are now poised to do something that’s truly on the up and up: improve the state-of-the-art for the treatment of mood-related psychiatric conditions. In particular, a number of psychedelics are currently being investigated for their effects on serotonin, a chemical that, among its many other functions, carries messages throughout the brain and nervous system, regulating mood.
“Psychedelics affect serotonin receptors much faster than common antidepressants and appear to act in a more targeted manner”
Kawashima points out, however, that it’s problematic to test psychedelics on humans because of their hallucinogenic side effects, and it’s hard to know what exactly they do to the brain because they may target circuits in the brain’s deep-seated regions, where neural activity is difficult to observe. “Zebrafish larvae, on the other hand, are transparent, making it possible to monitor drugs’ impact on specific brain cells and to correlate this with behavior.”
The present study was launched at the instigation of Dr. Dotan Braun, a psychiatrist who joined Kawashima’s lab in Weizmann’s Brain Sciences Department as a visiting scientist. Inspired by Kawashima’s technology for imaging brain activity in zebrafish and his investigations of the serotonin system, Braun proposed a project that would help clarify the precise effects of psychedelics on serotonin. This in turn might contribute to the development of potential psychedelic alternatives to the widely prescribed class of antidepressants known as serotonin-selective reuptake inhibitors, or SSRIs, which include such drugs as Cipralex and Prozac.
“SSRIs elevate serotonin levels throughout the brain,” Braun says. “Psychedelics, in contrast, affect serotonin receptors via a different, much faster mechanism and they appear to act on brain areas in a more targeted manner. A better understanding of their mechanism of action and a mapping of their influence on the brain may lead to more efficient drugs, with fewer side effects.”
Fish on drugs
The scientists designed an experiment that enabled them to “get into the head” of zebrafish soaked in a solution containing psilocybin, a mushroom-derived psychedelic compound being tested for use against depression that is not relieved by other medications. Following a four-hour psilocybin “bath,” the fish dove into Kawashima’s arena for behavioral experiments: a shallow pool of water that has attention-grabbing visual patterns projected onto its glass bottom.
After exposing the fish to a stressful situation – a sudden, temporary drop in water temperature – the researchers compared their behaviors to those of fish that had not taken a preparatory bath. “We wanted to see how psychedelics affect the fish’s stress response,” Kawashima says, adding with a smile: “We found that, similar to what can be true for humans, when you’re heading into a stressful situation, taking a long bath can help.”
Indeed, the psychedelic bath reduced stress-related behaviors in two ways. Following stress exposure, the presoaked fish were more likely to explore the tank, venturing even into its darker domains, compared to fish that were drug-free. The “drugged” fish also darted about faster than the “sober” ones. These differences suggested that psilocybin produced a stimulating effect.
In addition, psilocybin reduced post-stress anxiety. “Fish that had not bathed in psilocybin reacted to the sudden drop in temperature with irregular, zig-zag swimming,” says Ayelet Rosenberg, a research student in Kawashima’s lab who, together with Braun, is a first coauthor of the research paper. “But the fish that had been pretreated with the psychedelic drug stayed calm; they seemed to take this added stress in stride.”
The scientists were able to pick up on these differences in behavior by documenting freely swimming individual zebrafish in minute detail with the help of a high-speed camera that produced 270,000 images for each 15-minute experiment. A subset of this wealth of images was manually annotated for ten zebrafish body parts, including the eyes, nostril, body trunk, and six points along the tail, and used to train a deep neural network – an advanced AI algorithm – to identify the nuances of the fish’s swimming patterns. Once trained, the algorithm was able to identify complex swimming trajectories and map out how behavior changed in fish under the influence of psychedelics.
The scientists were then able to link these behavioral effects to specific neural activation patterns. They relied on a method, previously developed by Kawashima and colleagues, involving the fluorescent tagging of individual zebrafish neurons and neural circuits, which causes them to light up when activated. Because the zebrafish larvae are transparent, the scientists were able to use a powerful optical microscope to image this activation directly, enabling them to identify specific changes in serotonin-related neurons and circuits.
Over 100: number of visits, phone calls and emails to Israel’s Ministry of Health by members of Dr. Kawashima’s team before they received permission to use psilocybin, making theirs the first Israeli lab ever authorized to work with this controlled psychedelic substance.
“Our optical imaging has revealed neural activity patterns in psilocybin-soaked fish that were similar to those seen by other labs in the mammalian brain exposed to psychedelics,” says Kawashima. “This indicates that psilocybin exerts its influence on behavior through neural mechanisms in deep areas of the brain that have been conserved in evolution and are also found in mammals, including humans.”
A “trip” toward better psychiatric treatment
The Kawashima team’s methodology and findings could help advance the development of psychedelics as therapies for mood-related conditions. Kawashima cautions that studying psychedelics in fish has its limits: Despite the fascinating nature of the question, it is unclear, for example, whether zebrafish experience hallucinatory “trips” in the course of these investigations. Still, his method can help advance therapeutic research in psychiatry.
“The practical significance of our work is that it demonstrates a fish-based screening tool for drug discovery,” he says. “Researchers can use our method to test new drug compounds or compare the relative usefulness of the serotonin-targeting drugs already in use. This could lead to discoveries about the mechanics of serotonin-related disorders, something that could generate entirely new approaches to the treatment of depression, anxiety, OCD, PTSD and addiction.”
Dr. Takashi Kawashima is the incumbent of the Birnbach Family Career Development Chair.
His research is supported by the Swiss Society Center for Research on Perception and Action and the Jared M. Drescher Center for Research on Mental and Emotional Health.