Posts tagged science
Articles and news from the latest research reports.
Childhood’s end: ADHD, autism and schizophrenia tied to stronger inhibitory interactions in adolescent prefrontal cortex
Key cognitive functions such as working memory (which combines temporary storage and manipulation of information) and executive function (a set of mental processes that helps connect past experience with present action) are associated with the brain’s prefrontal cortex. Unlike other brain regions, the prefrontal cortex does not mature until early adulthood, with the most pronounced changes being seen between its peripubertal (onset of puberty) and postpubertal developmental states. Moreover, this maturation period is correlated with cognitive maturation – but the physical neuronal changes during this transition have remained for the most part unknown. Recently, however, scientists at the Wake Forest School of Medicine in Winston-Salem, NC recorded and compared prefrontal cortical activity peripubertal and adult monkeys.
The researchers found that compared with adults, peripubertal monkeys showed lower connectivity due to stronger inhibitory interactions, suggesting that intrinsic (or resting state) inhibitory connections – that is, inhibitory neural connections that are active in the absence of any particular task – decline with maturation. The scientists then concluded that prefrontal intrinsic connectivity changes are a possible substrate for cognitive maturation.
Prof. Christos Constantinidis discusses the paper that he, Dr. Xin Zhou and their co-authors published in Proceedings of the National Academy of Sciences. When comparing the functional connectivity between pairs of neurons in neuronal activity recorded from the prefrontal cortex of peripubertal and adult monkeys and evaluating the developmental stage of peripubertal rhesus monkeys with a series of morphometric, hormonal, and radiographic measures, Constantinidis tells Medical Xpress that a major challenge was to obtain neural activity from the brain of monkeys around the time of puberty. “We needed to make ourselves experts in the developmental trajectories of monkeys and conduct experiments just at the right time relative to the onset of puberty,” he explains.
Stumbling Fruit Flies Lead Scientists to Discover Gene Essential for Sensing Joint Position
Scientists at The Scripps Research Institute (TSRI) have discovered an important mechanism underlying sensory feedback that guides balance and limb movements.
The finding, which the TSRI team uncovered in fruit flies, centers on a gene and a type of nerve cell required for detection of leg-joint angles. “These cells resemble human nerve cells that innervate joints,” said team leader Professor Boaz Cook, who is an assistant professor at TSRI, “and they encode joint-angle information in the same way.”
If the findings can be fully replicated in humans, they could lead to a better understanding of, as well as treatments for, disorders arising from faulty proprioception, the detection of body position.
A report of the findings appears in the March 14, 2014 issue of the journal Science.
A Mystery of Sensation
The proprioceptive sense of how the limbs are positioned is what enables a person, even with eyes closed, to touch the tip of the nose with the tip of a finger—an ability easily impaired by alcohol, which is why traffic police often test suspected drunk drivers this way.
Scientists have known that proprioceptive signals originate from so-called mechanosensory neurons, whose nerve ends are embedded in muscles, skin and other tissues. The stretching or compression of these tissues opens ion channels in the nerve membrane, which results in a signal to the brain.
What hasn’t been clear is how such a neuron can specialize in sensing just one type of membrane-distorting stimulus—such as the angle of a limb joint—yet exclude others, such as impact pressures.
In the new study, Cook and two members of his laboratory, first author Bela S. Desai, a postdoctoral fellow, and graduate student Abhishek Chadha, sought to shed some light on this mystery with a study of Drosophila fruit flies. Quickly maturing and easily studied, Drosophila often are analyzed for clues to the genetic underpinnings of basic animal behaviors.
Following the Trail
Cook and his colleagues began with a special collection of Drosophila containing a variety of uncatalogued mutations. The scientists sifted through the collection looking for mutant flies with walking impairments and soon zeroed in on several impaired walkers that turned out to have mutations in the same gene.
The scientists named the gene stumble (stum for short) for the abnormality caused by its absence.
Using a fluorescent tracer, they then localized the expression of stum in normal flies to neurons that lay close to the three main leg joints. Each neuron’s input-sensing tendril (dendrite) grew right up to the joints—a sign that its evolved function is to detect joint angle.
The researchers also found that the protein specified by the stum gene normally migrates to the tip of each dendrite. With high-resolution microscopy, they imaged each of these tips and observed an extra length branching more or less sideways at the joint.
At ordinary, at-rest joint angles, the relative positions of the main dendrite tip and its side branch stayed more or less the same; however, at extreme joint angles, the pair stretched out. As they did, the level of calcium ions in the neuron rose sharply, suggesting that ion channels had opened and the neuron was becoming active.
Cook noted the results show how a seemingly general mechanosensory, membrane-stretch-sensitive neuron can evolve a specificity for a particular type of proprioceptive signal. “It’s a nice example of how you can create that specificity from something that only stretches mechanically,” he said.
The team is now trying to nail down the specific role of stum proteins in Drosophila and to determine whether the human version of stum—which has never been characterized—also works in joint angle sensing. Some sensory role for the human version of stum is likely, as the stum gene has been remarkably well conserved throughout animal evolution. Cook and his colleagues were even able to restore some normal walking ability to stum-mutant flies by adding the mouse version of the stum gene. “Stum is probably doing the same thing in all animals,” he said.
Researchers Identify Gene That Helps Fruit Flies Go to Sleep
A novel protein may explain how biological clocks regulate human sleep cycles
In a series of experiments sparked by fruit flies that couldn’t sleep, Johns Hopkins researchers say they have identified a mutant gene — dubbed “Wide Awake” — that sabotages how the biological clock sets the timing for sleep. The finding also led them to the protein made by a normal copy of the gene that promotes sleep early in the night and properly regulates sleep cycles.
Because genes and the proteins they code for are often highly conserved across species, the researchers suspect their discoveries — boosted by preliminary studies in mice — could lead to new treatments for people whose insomnia or off-hours work schedules keep them awake long after their heads hit the pillow.
“We know that the timing of sleep is regulated by the body’s internal biological clock, but just how this occurs has been a mystery,” says study leader Mark N. Wu, M.D., Ph.D., an assistant professor of neurology, medicine, genetic medicine and neuroscience at the Johns Hopkins University School of Medicine. “We have now found the first protein ever identified that translates timing information from the body’s circadian clock and uses it to regulate sleep.”
A report on the work was published online March 13 in the journal Neuron.
In their hunt for the molecular roots of sleep regulation, Wu and his colleagues studied thousands of fruit fly colonies, each with a different set of genetic mutations, and analyzed their sleep patterns. They found that one group of flies, with a mutation in the gene they would later call Wide Awake (or Wake for short), had trouble falling asleep at night, a malady that looked a lot like sleep-onset insomnia in humans. The investigators say Wake appears to be the messenger from the circadian clock to the brain, telling it that it’s time to shut down and sleep.
After isolating the gene, Wu’s team determined that when working properly, Wake helps shut down clock neurons of the brain that control arousal by making them more responsive to signals from the inhibitory neurotransmitter called GABA. Wake does this specifically in the early evening, thus promoting sleep at the right time. Levels of Wake cycle during the day, peaking near dusk in good sleepers.
Flies with a mutated Wake gene that couldn’t get to sleep were not getting enough GABA signal to quiet their arousal circuits at night, keeping the flies agitated.
The researchers found the same gene in every animal they studied: humans, mice, rabbits, chickens, even worms.
Importantly, when Wu’s team looked to see where Wake was located in the mouse brain, they found that it was expressed in the suprachiasmatic nucleus (SCN), the master clock in mammals. Wu says the fact that the Wake protein was expressed in high concentrations in the SCN of mice is significant.
“Sometimes we discover things in flies that have no direct relevance in higher order animals,” Wu says. “In this case, because we found the protein in a location where it likely plays a role in circadian rhythms and sleep, we are encouraged that this protein may do the same thing in mice and people.”
The hope is that someday, by manipulating Wake, possibly with a medication, shift workers, military personnel and sleep-onset insomniacs could sleep better.
“This novel pathway may be a place where we can intervene,” Wu says.
(Source: hopkinsmedicine.org)
What happened when? How the brain stores memories by time
Before I left the house this morning, I let the cat out and started the dishwasher. Or was that yesterday? Very often, our memories must distinguish not just what happened and where, but when an event occurred — and what came before and after. New research from the University of California, Davis, Center for Neuroscience shows that a part of the brain called the hippocampus stores memories by their “temporal context” — what happened before, and what came after.
"We need to remember not just what happened, but when," said graduate student Liang-Tien (Frank) Hsieh, first author on the paper published March 5 in the journal Neuron.
The hippocampus is thought to be involved in forming memories. But it’s not clear whether the hippocampus stores representations of specific objects, or if it represents them in context.
Hsieh and Charan Ranganath, professor in the Department of Psychology and the Center for Neuroscience, looked for hippocampus activity linked to particular memories. First, they showed volunteers a series of pictures of animals and objects. Then they scanned the volunteers’ brains as they showed them the same series again, with questions such as, “is this alive?” or “does this generate heat?”
The questions prompted the volunteers to search their memories for information. When the images were shown in the same sequence as before, the volunteers could anticipate the next image, making for a faster response.
From brain scans of the hippocampus as the volunteers were answering questions, Hsieh and Ranganath could identify patterns of activity specific to each image. But when they showed the volunteers the same images in a different sequence, they got different patterns of activity.
In other words, the coding of the memory in the hippocampus was dependent on its context, not just on content.
"It turns out that when you take the image out of sequence, the pattern disappears," Ranganath said. "For the hippocampus, context is critical, not content, and it’s fairly unique in how it pulls things together."
Other parts of the brain store memories of objects that are independent of their context, Ranganath noted.
"For patients with memory problems this is a big deal," Ranganath said. "It’s not just something that’s useful in understanding healthy memory, but allows us to understand and intervene in memory problems."
Researchers identify decision-making center of brain
Although choosing to do something because the perceived benefit outweighs the financial cost is something people do daily, little is known about what happens in the brain when a person makes these kinds of decisions. Studying how these cost-benefit decisions are made when choosing to consume alcohol, University of Georgia associate professor of psychology James MacKillop identified distinct profiles of brain activity that are present when making these decisions.
"We were interested in understanding how the brain makes decisions about drinking alcohol. Particularly, we wanted to clarify how the brain weighs the pros and cons of drinking," said MacKillop, who directs the Experimental and Clinical Psychopharmacology Laboratory in the UGA Franklin College of Arts and Sciences.
The study combined functional magnetic resonance imaging and a bar laboratory alcohol procedure to see how the cost of alcohol affected people’s preferences. The study group included 24 men, age 21-31, who were heavy drinkers. Participants were given a $15 bar tab and then were asked to make decisions in the fMRI scanner about how many drinks they would choose at varying prices, from very low to very high. Their choices translated into real drinks, at most eight that they received in the bar immediately after the scan. Any money not spent on drinks was theirs to keep.
The study applied a neuroeconomic approach, which integrates concepts and methods from psychology, economics and cognitive neuroscience to understand how the brain makes decisions. In this study, participants’ cost-benefit decisions were categorized into those in which drinking was perceived to have all benefit and no cost, to have both benefits and costs, and to have all costs and no benefits. In doing so, MacKillop could dissect the neural mechanisms responsible for different types of cost-benefit decision-making.
"We tried to span several levels of analysis, to think about clinical questions, like why do people choose to drink or not drink alcohol, and then unpack those choices into the underlying units of the brain that are involved," he said.
When participants decided to drink in general, activation was seen in several areas of the cerebral cortex, such as the prefrontal and parietal cortices. However, when the decision to drink was affected by the cost of alcohol, activation involved frontostriatal regions, which are important for the interplay between deliberation and reward value, suggesting suppression resulting from greater cognitive load. This is the first study of its kind to examine cost-benefit decision-making for alcohol and was the first to apply a framework from economics, called demand curve analysis, to understanding cost-benefit decision making.
"The brain activity was most differentially active during the suppressed consumption choices, suggesting that participants were experiencing the most conflict," MacKillop said. "We had speculated during the design of the study that the choices not to drink at all might require the most cognitive effort, but that didn’t seem to be the case. Once people decided that the cost of drinking was too high, they didn’t appear to experience a great deal of conflict in terms of the associated brain activity."
These conflicted decisions appeared to be represented by activity in the anterior insula, which has been linked in previous addiction studies to the motivational circuitry of the brain. Not only encoding how much people crave or value drugs, this portion of the brain is believed to be responsible for processing interceptive experiences, a person’s visceral physiological responses.
"It was interesting that the insula was sensitive to escalating alcohol costs especially when the costs of drinking outweighed the benefits," MacKillop said. "That means this could be the region of the brain at the intersection of how our rational and irrational systems work with one another. In general, we saw the choices associated with differential brain activity were those choices in the middle, where people were making choices that reflect the ambivalence between cost and benefits. Where we saw that tension, we saw the most brain activity."
While MacKillop acknowledges the impact this research could have on neuromarketing-or understanding how the brain makes decisions about what to buy-he is more interested in how this research can help people with alcohol addictions.
"These findings reveal the distinct neural signatures associated with different kinds of consumption preferences. Now that we have established a way of studying these choices, we can apply this approach to better understanding substance use disorders and improving treatment," he said, adding that comparing fMRI scans from alcoholics with those of people with normal drinking habits could potentially tease out brain patterns that show what is different between healthy and unhealthy drinkers. "In the past, we have found that behavioral indices of alcohol value predict poor treatment prognosis, but this would permit us to understand the neural basis for negative outcomes."
The research was published in the journal Neuropsychopharmacology March 3. A podcast highlighting this work is available at http://www.nature.com/multimedia/podcast/npp/npp_030314_alcohol.mp3.
New gene for bipolar disorder discovered
Team of researchers searched for the foundations of manic-depressive disorder in about 24,000 people
First on top of the world and then in the depths of despair – this is what the extreme mood changes for people with bipolar disorder are like. Under the direction of scientists from the University of Bonn Hospital, the Central Institute of Mental Health of Mannheim and the University of Basel Hospital, an international collaboration of researchers discovered two new gene regions which are connected with the prevalent disease. In addition, they were able to confirm three additional suspect genes. In this unparalleled worldwide study, the scientists are utilizing unprecedented numbers of patients. The results are now being published in the renowned journal “Nature Communications”.
Throughout the course of their lives, about one percent of the population suffers from bipolar disorder, also known as manic-depressive disorder. The patients undergo a veritable rollercoaster of emotions: During extreme shifts, they experience manic phases with delusions of grandeur, increased drive and a decreased need for sleep as well as depressive episodes with a severely depressed mood to the point of suicidal thoughts. The causes of the disease are not yet fully understood, however in addition to psychosocial triggers, genetic factors play a large role. “There is no one gene that has a significant effect on the development of bipolar disorder,” says Prof. Dr. Markus M. Nöthen, Director of the Institute of Human Genetics of the University of Bonn Hospital. “Many different genes are evidently involved and these genes work together with environmental factors in a complex way.”
Scale of the investigation is unparalleled worldwide
In recent years, scientists at the Institute of Human Genetics were already involved in decoding several genes associated with bipolar disorder. The researchers working with Prof. Dr. Marcella Rietschel from the Central Institute of Mental Health of Mannheim, Prof. Dr. Markus M. Nöthen from the University of Bonn Hospital and Prof. Dr. Sven Cichon from the University of Basel Hospital are now using unprecedented numbers of patients in an international research collaboration: New genetic data from 2266 patients with manic-depressive disorder and 5028 control persons were obtained, merged with existing data sets and analyzed together. In total, data on the genetic material of 9747 patients were compared with data from 14,278 healthy persons. “The investigation of the genetic foundations of bipolar disorder on this scale is unique worldwide to date,” says Prof. Rietschel from the Central Institute of Mental Health of Mannheim.
The search for genes involved in manic-depressive disorder is like looking for a needle in a haystack. “The contributions of individual genes are so minor that they normally cannot be identified in the ‘background noise’ of genetic differences,” explains Prof. Cichon from the University of Basel Hospital. Only when the DNA from very large numbers of patients with bipolar disorder are compared to the genetic material from an equally large number of healthy persons can differences be confirmed statistically. Such suspect regions which indicate a disease are known by scientists as candidate genes.
Two new gene regions discovered and three known gene regions confirmed
Using automated analysis methods, the researchers recorded about 2.3 million different regions in the genetic material of patients and comparators, respectively. The subsequent evaluation using biostatistical methods revealed a total of five risk regions on the DNA associated with bipolar disorder. Two of these regions were newly discovered: The gene “ADCY2” on chromosome five and the so-called “MIR2113-POU3F2” region on chromosome six. The risk regions “ANK3”, “ODZ4” and “TRANK1” have already been described in prior studies. “These gene regions were, however, statistically better confirmed in our current investigation - the connection with bipolar disorder has now become even clearer,” says Prof. Nöthen.
The researchers are particularly interested in the newly discovered gene region “ADCY2”. It codes an enzyme which is involved in the conduction of signals into nerve cells. “This fits very well with observations that the signal transfer in certain regions of the brain is impaired in patients with bipolar disorder,” explains the human geneticist of the University of Bonn Hospital. With their search for genetic regions, the scientists are gradually clarifying the causes of manic-depressive disorder. “Only when we know the biological foundations of this disease can be also identify starting points for new therapies,” says Prof. Nöthen.
(Image caption: Illustration of the mirror neuron system in the human brain. Credit: Jan Brascamp)
Brain mapping confirms patients with schizophrenia have impaired ability to imitate
According to George Bernard Shaw, “Imitation is not just the sincerest form of flattery – it’s the sincerest form of learning.” According to psychologists, imitation is something that we all do whenever we learn a new skill, whether it is dancing or how to behave in specific social situations.
Now, the results of a brain-mapping experiment conducted by a team of neuroscientists at Vanderbilt University strengthen the theory that an impaired ability to imitate may underlie the profound and enduring difficulty with social interactions that characterize schizophrenia. In a paper published online on Mar. 14 by the American Journal of Psychiatry, the researchers report that when patients with schizophrenia were asked to imitate simple hand movements, their brains exhibited abnormal brain activity in areas associated with the ability to imitate.
“The fact that patients with schizophrenia show abnormal brain activity when they imitate simple hand gestures is important because action imitation is a primary building block of social abilities,” said first author Katharine Thakkar, who conducted much of the research while completing her doctoral program at Vanderbilt and is now a post-doctoral fellow at the University Medical Center in Utrecht. “The ability to imitate is present early in life and is crucial for learning how to navigate the social world. According to current theory, covert imitation is also the most fundamental way that we understand the intentions and feelings of other people.”
Contagious Yawning May Not Be Linked to Empathy; Still Largely Unexplained
While previous studies have suggested a connection between contagious yawning and empathy, new research from the Duke Center for Human Genome Variation finds that contagious yawning may decrease with age and is not strongly related to variables like empathy, tiredness and energy levels.
The study, published March 14 in the journal PLOS ONE, is the most comprehensive look at factors influencing contagious yawning to date.
The researchers said a better understanding of the biology involved in contagious yawning could ultimately shed light on illnesses such as schizophrenia or autism.
“The lack of association in our study between contagious yawning and empathy suggests that contagious yawning is not simply a product of one’s capacity for empathy,” said study author Elizabeth Cirulli, Ph.D., assistant professor of medicine at the Center for Human Genome Variation at Duke University School of Medicine.
Contagious yawning is a well-documented phenomenon that occurs only in humans and chimpanzees in response to hearing, seeing or thinking about yawning. It differs from spontaneous yawning, which occurs when someone is bored or tired. Spontaneous yawning is first observed in the womb, while contagious yawning does not begin until early childhood.
Why certain individuals are more susceptible to contagious yawning remains poorly understood. Previous research, including neuroimaging studies, has shown a relationship between contagious yawning and empathy, or the ability to recognize or understand another’s emotions. Other studies have shown correlations between contagious yawning and intelligence or time of day.
Interestingly, people with autism or schizophrenia, both of which involve impaired social skills, demonstrate less contagious yawning despite still yawning spontaneously. A deeper understanding of contagious yawning could lead to insights on these diseases and the general biological functioning of humans.
The current study aimed to better define how certain factors affect someone’s susceptibility to contagious yawning. The researchers recruited 328 healthy volunteers, who completed cognitive testing, a demographic survey, and a comprehensive questionnaire that included measures of empathy, energy levels and sleepiness.
The participants then watched a three-minute video of people yawning, and recorded the number of times they yawned while watching the video.
The researchers found that certain individuals were less susceptible to contagious yawns than others, with participants yawning between zero and 15 times during the video. Of the 328 people studied, 222 contagiously yawned at least once. When verified across multiple testing sessions, the number of yawns was consistent, demonstrating that contagious yawning is a very stable trait.
In contrast to previous studies, the researchers did not find a strong connection between contagious yawning and empathy, intelligence or time of day. The only independent factor that significantly influenced contagious yawning was age: as age increased, participants were less likely to yawn. However, age was only able to explain 8 percent of the variability in the contagious yawn response.
“Age was the most important predictor of contagious yawning, and even age was not that important. The vast majority of variation in the contagious yawning response was just not explained,” Cirulli said.
Because most variability in contagious yawning remains unexplained, the researchers are now looking to see whether there are genetic influences that contribute to contagious yawning. Their long-term goal in characterizing variability in contagious yawning is to better understand human diseases like schizophrenia and autism, as well as general human functioning, by identifying the genetic basis of this trait.
“It is possible that if we find a genetic variant that makes people less likely to have contagious yawns, we might see that variant or variants of the same gene also associated with schizophrenia or autism,” Cirulli said. “Even if no association with a disease is found, a better understanding of the biology behind contagious yawning can inform us about the pathways involved in these conditions.”
Critical role of one gene to our brain development
New research from the University of Adelaide has confirmed that a gene linked to intellectual disability is critical to the earliest stages of the development of human brains.
Known as USP9X, the gene has been investigated by Adelaide researchers for more than a decade, but in recent years scientists have begun to understand its particular importance to brain development.
In a new paper published online in the American Journal of Human Genetics, an international research team led by the University of Adelaide’s Robinson Research Institute explains how mutations in USP9X are associated with intellectual disability. These mutations, which can be inherited from one generation to the next, have been shown to cause disruptions to normal brain cell functioning.
Speaking during Brain Awareness Week, senior co-author Dr Lachlan Jolly from the University of Adelaide’s Neurogenetics Research Program says the USP9X gene has shed new light on the mysteries of brain development and disability.
Dr Jolly says the base framework for the brain’s complex network of cells begins to form at the embryo stage.
"Not surprisingly, disorders that cause changes to this network of cells, such as intellectual disabilities, epilepsy and autism, are hard to understand, and treat," Dr Jolly says.
"By looking at patients with severe learning and memory problems, we discovered a gene - called USP9X - that is involved in creating this base network of nerve cells. USP9X controls both the initial generation of the nerve cells from stem cells, and also their ability to connect with one another and form the proper networks,” he says.
"This work is critical to understanding how the brain develops, and how it is altered in individuals with brain disorders.
"We hope that by learning more about genes such as USP9X, we will create new opportunities to understand brain disorders at a much deeper level than currently known, which could lead to future treatment opportunities.”
How a small worm may help the fight against Alzheimer’s
Scientists at the Max Planck Institute for Biology of Ageing in Cologne have found that a naturally occurring molecule has the ability to enhance defense mechanisms against neurodegenerative diseases. Feeding this particular metabolite to the small round worm Caenorhabditis elegans, helps clear toxic protein aggregates in the body and extends life span.
During ageing, proteins in the human body tend to aggregate. At a certain point, protein aggregation becomes toxic, overloads the cell, and thus prevents it from maintaining normal function. Damage can occur, particularly in neurons, and may result in neurodegenerative diseases like Alzheimer’s, Parkinson’s or Huntington’s disease. By studying model organisms like Caenorhabditis elegans, scientists have begun to uncover the mechanisms underlying neurodegeneration, and thus define possible targets for both therapy and prevention of those diseases. “Although we cannot measure dementia in worms“, explains Martin Denzel of the Max Planck Institute for Biology of Ageing, “we can observe proteins that we also know from human diseases like Alzheimer’s to be toxic by measuring effects on neuromuscular function. This gives us insight into how Alzheimer actually progresses on the molecular level“.
Now, the scientists Martin Denzel, Nadia Storm, and Max Planck Director Adam Antebi have discovered that a substance called N-acetylglucosamine apparently stimulates the body’s own defense mechanism against such toxicity. This metabolite occurs naturally in the organism. If it is additionally fed to the worm, “we can achieve very dramatic benefits“, says Denzel. “It is a broad-spectrum effect that alleviates protein toxicity in Alzheimer’s, Parkinson’s and Huntington’s disease models in the worm, and it even extends their life span.“
This molecule apparently plays a crucial role in quality control mechanisms that keep the body healthy. It helps the organism to clear toxic levels of protein aggregation, both preventing aggregates from forming and clearing already existing ones. As a result, onset of paralysis is delayed in models of neurodegeneration - How exactly the molecule achieves this effect is yet to be uncovered. “And we still don’t know whether it also works in higher animals and humans“, says Antebi. “But as we also have these metabolites in our cells, this gives good reason to suspect that similar mechanisms might work in humans.”