The gene to which we owe our big brain

A section of a brain organoid made from stem cells of a human. In magenta are actively proliferating brain stem cells, in yellow a subset of brain stem cells.
Photo Credit: Jan Fischer

ARHGAP11B - this complex name is given to a gene that is unique to humans and plays an essential role in the development of the neocortex. The neocortex is the part of the brain to which we owe our high mental abilities. A team of researchers from the German Primate Center (DPZ) - Leibniz Institute for Primate Research in Göttingen, the Max Planck Institute for Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, and the Hector Institute for Translational Brain Research (HITBR) in Mannheim has investigated the importance of ARHGAP11B in neocortex development during human evolution. 

To do this, the team introduced for the first time a gene that exists only in humans into laboratory-grown brain organoids from our closest living relatives, chimpanzees. In the chimpanzee brain organoid, the ARHGAP11B gene led to an increase in brain stem cells relevant to brain growth and an increase in those neurons that play a critical role in the extraordinary mental abilities of humans. If, on the other hand, the ARHGAP11B gene was switched off in human brain organoids, the quantity of these brain stem cells fell to the level of a chimpanzee. Thus, the research team was able to show that the ARGHAP11B gene played a crucial role in the evolution of the brain from our ancestors to modern humans.

New study finds subtle structural brain alterations in youth with suicidal behaviors

ENGIMA-STB aims to identify neurobiological variations associated with suicidal ideations and behaviors, to ultimately leverage information from brain structure, function, along with clinical and demographic factors, to predict the likelihood of a future suicidal attempt.
Image credit: USC Stevens INI

The ENIGMA Suicidal Thoughts and Behaviors (ENIGMA-STB) consortium gathered and analyzed neuroimaging data from 18 different studies worldwide to examine associations between brain structure and suicide attempt in young people with major depressive disorder.

Suicide is the second leading cause of death in the United States for young people from the age of 10 up to 33. Tragically, the number of suicide attempts among children and adolescents has continued to increase despite national and international prevention efforts. Collaborative research where specialists all over the world work together is needed to advance our understanding of the complex nature of suicidal thoughts and behaviors, and ultimately, to develop better interventions and preventions.

A new study by a global team of researchers including Neda Jahanshad, PhD, of the Keck School of Medicine of USC’s Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI), has revealed subtle alterations in the size of the brain’s prefrontal region in young people with mood disorders and suicidal thoughts and behaviors. The study was recently published in Molecular Psychiatry.

New knowledge about the link between infection during pregnancy and autism

Credit: Mart Production

Infections in pregnant women have been linked to increased risk of neuropsychiatric conditions, such as autism, in the child later in life. But it does not appear to be the infections themselves that cause autism, researchers from Karolinska Institutet show in a study published in The Lancet Psychiatry.

Our results can reassure future parents by showing that infections during pregnancy may not pose as much risk to the child's brain as previously thought, say Håkan Karlsson, researchers at Department of Neuroscience at Karolinska Institutet and the study's last author.

Previous studies have shown a link between infections of the future mother during pregnancy and increased risk of autism and intellectual disability in the child later in life.

But they have not been able to say whether it is really the infection of the mother that is the cause, or whether other factors are behind it. Researchers from Karolinska Institutet have now studied this more closely.

How Fat Signals Us to Eat More of It

Charles S. Zuker
Columbia University Neuroscience Physiology
Source: HHMI

Scientists discover how fat triggers a gut-to-brain mechanism that drives us to keep consuming more of it. Their findings could one day lead to interventions to help treat obesity and associated disorders.

Short ribs glazed in a sweet sticky sauce and slow-cooked to perfection, potato chips hand-fried and tossed with a generous coating of sour cream, chicken wings battered and double-fried so that they stay crispy for hours. What is it about these, and other, mouth-watering — but incredibly fatty — foods that makes us reach out, and keep coming back for more?

How they taste on the tongue is one part of the story, but to really understand what drives “our insatiable appetite for fat,” we have to examine what happens after fat is consumed, says Columbia University’s Charles Zuker, a neuroscientist and molecular geneticist who has been a Howard Hughes Medical Institute (HHMI) Investigator since 1989.

Two years ago, Zuker and his team reported how sugar, upon reaching the gut, triggers signals that are sent to the brain, thus fueling cravings for sweet treats. Now, in an article published in Nature on September 7, 2022, they describe a similar gut-to-brain circuit that underlies a preference for fat.

“The gut is the source of our great desire for fat and sugar,” says Zuker.

The topic in question is an incredibly timely one, given the current global obesity epidemic. An estimated 13 percent of adults worldwide are obese — thrice that in 1975. In the US, that figure is even higher — at a staggering 42 percent. “It’s a very significant and important health problem,” says Zuker.

Having a high body-mass index is a risk factor for stroke, diabetes, and several other diseases. “It’s clear that if we want to help make a difference here, we need to understand the biological basis for our strong appetite for fat and sugar,” he says. Doing so will help us design interventions in the future to “suppress this strong drive to consume” and combat obesity.

How does nature nurture the brain?

Credit: Jessica Rockowitz on Unsplash

After a 60-minute walk in nature, activity in brain regions involved in stress processing decreases. This is the finding of a recent study by the Lise Meitner Group for Environmental Neuroscience at the Max Planck Institute for Human Development, published in Molecular Psychiatry.

Living in a city is a well-known risk factor for developing a mental disorder, while living close to nature is largely beneficial for mental health and the brain. A central brain region involved in stress processing, the amygdala, has been shown to be less activated during stress in people who live in rural areas, compared to those who live in cities, hinting at the potential benefits of nature. “But so far the hen-and-egg problem could not be disentangled, namely whether nature actually caused the effects in the brain or whether the particular individuals chose to live in rural or urban regions”, says Sonja Sudimac, predoctoral fellow in the Lise Meitner Group for Environmental Neuroscience and lead author of the study.

To achieve causal evidence, the researchers from the Lise Meitner Group for Environmental Neuroscience examined brain activity in regions involved in stress processing in 63 healthy volunteers before and after a one-hour walk in Grunewald forest or a shopping street with traffic in Berlin using functional magnetic resonance imaging (fMRI). The results of the study revealed that activity in the amygdala decreased after the walk in nature, suggesting that nature elicits beneficial effects on brain regions related to stress.

Cannabis users no less likely to be motivated or able to enjoy life’s pleasure

Credit: RODNAE Productions

Cannabis users also show no difference in motivation for rewards, pleasure taken from rewards, or the brain’s response when seeking rewards, compared to non-users.

Cannabis is the third most commonly used controlled substance worldwide, after alcohol and nicotine. A 2018 report from the NHS Digital Lifestyles Team stated that almost one in five (19%) of 15-year-olds in England had used cannabis in the previous 12 months, while in 2020 the National Institute on Drug Abuse reported the proportion in the United States to be 28% of 15-16-year-olds.

A common stereotype of cannabis users is the ‘stoner’ – think Jesse Pinkman in Breaking Bad, The Dude in The Big Lebowski, or, more recently, Argyle in Stranger Things. These are individuals who are generally depicted as lazy and apathetic.

At the same time, there has been considerable concern of the potential impact of cannabis use on the developing brain and that using cannabis during adolescence might have a damaging effect at an important time in an individual’s life.

A team led by scientists at UCL, the University of Cambridge and the Institute of Psychiatry, Psychology & Neuroscience at King’s College London carried out a study examining whether cannabis users show higher levels of apathy (loss of motivation) and anhedonia (loss of interest in or pleasure from rewards) when compared to controls and whether they were less willing to exert physical effort to receive a reward. The research was part of the CannTEEN study.

Study finds tiny brain area controls work for rewards

The lateral habenula in the mouse brain, with axons streaming down to dopaminergic and serotonergic centers. Credit: Warden Lab

A tiny but important area in the middle of the brain acts as a switch that determines when an animal is willing to work for a reward and when it stops working, according to a study published Aug. 31 in the journal Current Biology.

“The study changes how we think about this particular brain region,” said senior author Melissa Warden, assistant professor and Miriam M. Salpeter Fellow in the Department of Neurobiology and Behavior, which is shared between the College of Arts and Sciences and the College of Agriculture and Life Sciences.

“It has implications for psychiatric disorders, particularly depression and anxiety,” Warden said.

The paper, “Tonic Activity in Lateral Habenula Neurons Acts as a Neutral Valence Brake on Reward-Seeking Behavior,” illuminates the role of the lateral habenula, a small structure on top of the thalamus, which funnels higher-level information from the front and center of the brain to areas that produce neurotransmitters such as serotonin and dopamine.

The lateral habenula’s exact role has been unclear until now. The new study shows that when neurons in this brain area turn off, an animal will work for rewards; when those neurons fire, the animal becomes disengaged and stops working. Experiments revealed that the lateral habenula turns on specifically when an animal has had enough of a reward and is satisfied, or when it finds its work no longer yields a reward.

Brain activity during sleep differs in young people with genetic risk of psychiatric disorders

Photo by Lux Graves on Unsplash

Young people living with a genetic alteration that increases the risk of psychiatric disorders have markedly different brain activity during sleep, a study led by researchers from the Universities of Bristol and Cardiff published in the journal eLife shows.

The brain activity patterns during sleep shed light on the neurobiology behind a genetic condition called 22q11.2 Deletion Syndrome (22q11.2DS) and could be used as a biomarker to detect the onset of neuropsychiatric disorders in people with 22q11.2DS.

Caused by a gene deletion of around 30 genes on chromosome 22, 22q11.2DS occurs in one in 3000 births. It increases the risk of intellectual disability, autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD) and epileptic seizures. It is also one of the largest biological risk factors for schizophrenia. However, the biological mechanisms underlying psychiatric symptoms in 22q11.2DS are unclear.

Marianne van den Bree, co-senior author and Professor of Psychological Medicine at Cardiff said: “We have recently shown that the majority of young people with 22q11.2DS have sleep problems, particularly insomnia and sleep fragmentation, that are linked with psychiatric disorders. However, our previous analysis was based on parents reporting on sleep quality of their children, and the neurophysiology – what’s happening to brain activity – has not yet been explored.”

3D imaging contributes to a better understanding of early stages of Alzheimer's disease

Three-dimensional image of noradrenergic nerve cells in the envelope of locus coeruleus.
Photo credit: Gilvesy et al.

With the help of a new imaging technique for 3D, researchers at Karolinska Institutet, among others, have been able to characterize a part of the brain that shows the most accumulation of tau protein, an important biomarker for the development of Alzheimer's disease. The results published in the journal Acta Neuropathologica may in the future make it possible to have a more accurate neuropathological diagnosis of Alzheimer's disease spectrum at a very early stage.

Intracellular accumulation of pathological tau protein in the brain is a hallmark of several age-related neurodegenerative diseases, including Alzheimer's disease, which accounts for 60-80 percent of all dementia cases worldwide.

In a new study, researchers at Karolinska Institutet, SciLifeLab in Stockholm and several universities from Hungary, Canada, Germany and France have applied a state-of-the-art immune imaging technology, in combination with light sheet microscopy, to investigate a human brain stem core, locus coeruleus, which is an important core in the mammalian brain.

Sleepless and selfish: Lack of sleep makes us less generous

The new study shows how sleep loss dramatically reduces the desire to help others, triggered by a breakdown in the activity of key prosocial brain networks.
Image credit: Eti Ben Simon and Matthew Walker, UC Berkeley

Humans help each other — it’s one of the foundations of civilized society. But a new study by scientists at the University of California, Berkeley, reveals that a lack of sleep blunts this fundamental human attribute, with real-world consequences.

Lack of sleep is known to be associated with an increased risk of cardiovascular disease, depression, diabetes, hypertension and overall mortality. However, these new discoveries show that a lack of sleep also impairs our basic social conscience, making us withdraw our desire and willingness to help other people.

In one portion of the new study, the scientists showed that charitable giving in the week after the beginning of Daylight-Saving Time, when residents of most states “spring forward” and lose one hour of their day, dropped by 10% — a decrease not seen in states that do not change their clocks or when states return to standard time in the fall.

The study, led by UC Berkeley research scientist Eti Ben Simon and Matthew Walker, a UC Berkeley professor of psychology, adds to a growing body of evidence demonstrating that inadequate sleep not only harms the mental and physical well-being of an individual, but also compromises the bonds between individuals — and even the altruistic sentiment of an entire nation.

Researchers reprogram human skin cells to aged neurons to study neurodegenerative disorders

CC0 Public Domain

Researchers at Lund University in Sweden have developed a new method for studying age-related brain disorders. The researchers have focused on the neurodegenerative disorder Huntington’s disease and the results have now been published in the journal Brain.

Basic medical research often faces the challenge of developing disease models that correspond to specific disease mechanisms or the disease to be studied. This is a challenge that needs to be solved in order to produce new effective treatments. One example of a disease that is difficult to model for an understanding of the underlying mechanisms is Huntington’s disease. In part, this is due to the difficulty in recreating adequate animal or cellular models.

By reprogramming skin cells into neurons, Johan Jakobsson and his research group have been able to study Huntington’s disease in an innovative way that he believes could be significant for successful studies of several age-related brain disorders.

“We took skin biopsies from patients living with Huntington’s disease and reprogrammed the skin biopsies into neurons. We then compared these neurons with reprogrammed neurons from healthy people. The results are very interesting. We have found several defects that explain some of the disease mechanisms in neurons from patients with Huntington’s disease. Among other things, we observed that neurons from patients with Huntington’s disease show problems in breaking down and recycling a particular kind of protein – which can lead to a lack of energy in these cells”, says Johan Jakobsson, professor of neuroscience at Lund University.

Ageing neutralizes sex differences in the brain

When male and female fruit flies age, their brains become desexualized.
Credit: Erik Karits on Unsplash

When male and female fruit flies age, their brains become desexualized. Age-related changes take place in both sexes, but the male brain becomes feminized to a larger extent than the female brain becomes masculinized. This is the conclusion of a study performed by a research group at Linköping University.

It is a well-known fact that weaker individuals cannot afford to “invest” in sexual behaviors to the same extent as their healthier conspecifics. However, it is not clear if ageing, which weakens individuals, also leads to a reduced investment in sexual activities. You might think that for individuals close to the end of their lives, going “all in” on reproduction, in order to pass on their genes before it is too late, would be best. Sexual behaviors are directed from the brain, and to find out what happens to sex differences in this tissue when fruit flies age the researchers have investigated how genes expressed to different degrees in young males and females change over time.

“Our results show that gene expression in male and female brains become more similar with age, and that both sexes contribute to this pattern”, says Dr Antonino Malacrinò, one of the study’s main authors who now works at the University of Reggio Calabria in Italy.

What the study shows is that if the expression of a certain gene is higher in the brains of young females than in young males, the gene’s expressions is reduced in older females and increased in old males – and vice versa for genes with higher expression in young males.

“The results also show that the changes are larger in males than in females”, says Antonino Malacrinò.

Secret behind ‘nic-sickness’ could help break tobacco addiction

Nicotine is addictive because it activates the brain’s dopamine network, which makes us feel good. UC Berkeley researchers now show in experiments on mice that nicotine in high doses also activates a recently discovered dopamine network that responds to unpleasant stimuli. This aversive dopamine network could be leveraged to create a therapy that boosts the negative effects and lessens the rewards of nicotine.
Image credit: Christine Liu, UC Berkeley

If you remember your first hit on a cigarette, you know how sickening nicotine can be. Yet, for many people, the rewards of nicotine outweigh the negative effects of high doses.

University of California, Berkeley, researchers have now mapped out part of the brain network responsible for the negative consequences of nicotine, opening the door to interventions that could boost the aversive effects to help people quit smoking.

Though most addictive drugs at high doses can cause physiological symptoms that lead to unconsciousness or even death, nicotine is unique in making people physically ill when inhaled or ingested in large quantities. As a result, nicotine overdoses are rare, though the advent of e-cigarettes has made “nic-sick” symptoms like nausea and vomiting, dizziness, rapid heartbeat and headaches more common.

New research, conducted in mice, suggests that this aversive network could be manipulated to treat nicotine dependence.

“Decades of research have focused on understanding how nicotine reward leads to drug addiction and what are the underlying brain circuits. In contrast, the brain circuits that mediate the aversive effects of nicotine are largely understudied,” said Stephan Lammel, UC Berkeley associate professor of molecular and cell biology. “What we found is that the brain circuits that are activated after a high aversive dose are actually different from those that are activated when nicotine is delivered at a low dose. Now that we have an understanding of the different brain circuits, we think we can maybe develop a drug so that, when nicotine is taken at a low dose, these brain circuits can be coactivated to induce an acute aversive effect. This could actually be a very effective treatment for nicotine addiction in the future, which we currently do not have.”

A role for cell ‘antennae’ in managing dopamine signals in the brain

Microscope image of a cultured mouse neuron from the striatum region of the brain labeled with a green fluorescent antibody that detects dopamine receptor 1. The receptor localizes along the cell surface and is enriched in a primary cilium projecting from the cell body. Nuclei are indicated in blue.
 Credit: Image courtesy of Kirk Mykytyn

A historically overlooked rod-like projection present on nearly every cell type in the human body may finally be getting its scientific due: A new study has found that these appendages, called cilia, on neurons in the brain have a key role in ensuring a specific dopamine receptor’s signals are properly received.

The research was conducted in mouse models of a disorder called Bardet-Biedl syndrome, and applies to one of five proteins that regulate dopamine signaling, called dopamine receptor 1. In certain regions of the brain, this receptor can be thought of as an “on” switch that initiates motivated behavior – basically any behavior linked to pursuit of a goal.

The study showed that if the receptor either gets stuck on cilia or never has a chance to localize to these cell “antennae,” messages telling the body to move are reduced.

“There’s something about dopamine receptor 1 needing to get to and from neuronal cilia that’s required for proper signaling,” said lead author Kirk Mykytyn, associate professor of biological chemistry and pharmacology in The Ohio State University College of Medicine. “This is the first demonstration that cilia are important for dopamine receptor 1 signaling.”

When a task adds more steps, this circuit helps you notice

In their study, researchers traced neurons projecting from the anterior cingulate cortex (right, red) to the motor cortex (left, green). Note the images are at different scales.
Source: Picower Institute for Learning and Memory

Life is full of processes to learn and then relearn when they become more elaborate. One day you log in to an app with just a password, then the next day you also need a code texted to you. One day you can just pop your favorite microwavable lunch into the oven for six straight minutes, but then the packaging changes and you have to cook it for three minutes, stir, and then heat it for three more. Our brains need a way to keep up. A new study by neuroscientists at The Picower Institute for Learning and Memory at MIT reveals some of the circuitry that helps a mammalian brain learn to add steps.

In Nature Communications the scientists report that when they changed the rules of a task, requiring rats to adjust from performing just one step to performing two, a pair of regions on the brain’s surface, or cortex, collaborated to update that understanding and change the rats’ behavior to fit the new regime. The anterior cingulate cortex (ACC) appeared to recognize when the rats weren’t doing enough and updated cells in the motor cortex (M2) to adjust the task behavior.

“I started this project about 7 or 8 years ago when I wanted to study decision making.” said Daigo Takeuchi, a researcher at the University of Tokyo who led the work as a postdoc at the RIKEN-MIT Laboratory for Neural Circuit Genetics at The Picower Institute directed by senior author and Picower Professor Susumu Tonegawa. “New studies were finding a role for M2. I wanted to study what upstream circuits were influencing this.”

How bat brains listen out for incoming signals during echolocation

Bats "see" with the ears. Scientists at Goethe University have found out how the auditory cortex is prepared for the incoming acoustic signals.
Credit: Hechavarria

When bats emit sounds for echolocation, a feedback loop modulates the sensitivity of the auditory cortex for incoming acoustic signals. Neuroscientists from the Goethe University Frankfurt found out. In a study published in the journal "Nature Communications", they show that the flow of information in the neuronal circuit involved reversed as the sound was generated. This feedback prepares the auditory cortex for the expected “echoes” of the sounds sent out. The researchers see their results as a sign that the importance of feedback loops in the brain is currently still underestimated.

Bats are famous for their ultrasound navigation: they orientate themselves through their extremely sensitive hearing by emitting ultrasound sounds and getting a picture of their environment based on the sound thrown back. For example, the eyelid nose bat (Carollia perspicillata) the fruits she prefers as food through this echolocation system. At the same time, the bats also use their voice to communicate with their peers, for which they choose a somewhat lower frequency range.

Neuroscientist Julio C. Hechavarria from the Institute for Cell Biology and Neuroscience at Goethe University, together with his team, examines which brain activities in the case of the eyewear nose go hand in hand with the vocalizations. In their latest study, the Frankfurters examined how the front lobes - a region in the front brain that is associated with the planning of actions in humans - and the auditory cortex, in which acoustic signals are processed, work together in the echolocation. For this purpose, the researchers used tiny electrodes on the bats, which recorded the activity of the nerve cells in the frontal lobe and in the auditory cortex.

Brain imaging links stimulant-use relapse to distinct nerve pathway

Researchers used advanced brain imaging techniques to study nerve fibers connecting to the nucleus accumbens, which plays an important role in motivation and addiction.
Credit: Loreen Tisdall and Kelly H. MacNiven.

You might assume that people who are most prone to developing a substance use disorder in the first place would also have the hardest time avoiding relapse following treatment. But a new study by scientists with the Wu Tsai Neurosciences Institute’s NeuroChoice Initiative reveals that relapse may be linked to quite different brain circuits than addiction itself.

“There’s a huge revolving door problem with relapse,” said Brian Knutson, a professor of psychology. “These findings suggest ​​that what gets you into taking drugs may not be the same processes that get you out of it, which could be very valuable to help predict who is at highest risk of relapse coming out of treatment.”

Drug addiction presents a major global challenge. More than 35 million people worldwide self-report problematic use of drugs and admissions to drug treatment programs have surged in the United States in recent years. For many drugs, in particular stimulants such as cocaine and amphetamines, relapse remains a common problem. For example, as many as 50 percent of people with stimulant use disorders relapse within 6 months of release from treatment.

“The statistics are disheartening,” said Kelly MacNiven, a social science research scholar in the Knutson lab and co-author of the new study. “Unfortunately not much is known at a biological level about the drivers of relapse — understanding this better is going to be the first step to developing better ways to help people get out of dependence.”

Gene discovery indicates motor neuron diseases caused by abnormal lipid processing in cells

A new genetic discovery adds weight to a theory that motor neuron degenerative diseases are caused by abnormal lipid (fat) processing pathways inside brain cells. This theory will help pave the way for new diagnostic approaches and treatments for this group of conditions. The discovery will provide answers for certain families who have previously had no diagnosis.

Motor neuron degenerative diseases (MNDs) are a large family of neurological disorders. Currently, there are no treatments available to prevent onset or progression of the condition. MNDs are caused by changes in one of numerous different genes. Despite the number of genes known to cause MNDs, many patients remain without a much-needed genetic diagnosis.

The team behind the current work developed a hypothesis to explain a common cause of MNDs stemming from their discovery of 15 genes responsible for MNDs. The genes they identified are all involved in processing lipids - in particular cholesterol – inside brain cells. Their new hypothesis, published in the journal Brain, describes the specific lipid pathways that the team believe are important in the development of MNDs.

Now, the team has identified a further new gene – named TMEM63C – which causes a degenerative disease that affects the upper motor neuron cells in the nervous system. Also published in Brain, their latest discovery is important as the protein encoded by TMEM63C is located in the region of the cell where the lipid processing pathways they identified operate. This further bolster the hypothesis that MNDs are caused by abnormal processing of lipids including cholesterol.

“This new gene finding is consistent with our hypothesis that the correct maintenance of specific lipid processing pathways is crucial for the way brain cells function, and that abnormalities in these pathways are a common linking theme in motor neuron degenerative diseases,” said study co-author Professor Andrew Crosby from the University of Exeter. “It also enables new diagnoses and answers to be readily provided for families affected by some forms of MND”

New imaging technique to find out what happens in the brains of dogs and cats

In a preliminary experiment, Parkkonen held a quantum optical MEG sensor with his hand on his family cat’s, Roosa’s, head while she listened to simple sound sequences.
Credit: Professor Lauri Parkkonen / Aalto University

For years, Professor Lauri Parkkonen's team at Aalto University has been developing quantum optical sensors for measuring the brain's magnetic fields using a technique known as magnetoencephalography (MEG). In traditional MEG, the superconducting sensors operate at very low temperatures and need centimeters of thermal insulation, but the quantum optical sensors work at room temperature, so they can be placed directly on the surface of the head. This allows more accurate measurements of the brain’s magnetic fields.

Parkkonen and his team plan to use the new method to build on their earlier work measuring brain activity in cats and dogs. Now they plan to characterize the complexity of the temporal structures in sensory stimuli that cat and dog brains can track. Similar experiments in humans have found that our brain produces specific responses to deviations in complex structures only when we attend to the stimuli and become aware of the deviations. Once the technique is perfected, Parkkonen and his team plan to use it to make similar measurements in human babies.

The experiments will begin this autumn – though Parkkonen has already done some preliminary tests with his family cat, Roosa – and the project is expected to continue until 2026. The researchers hope that their findings will provide an unprecedented window onto the cognition of cats and dogs, and this could also help bridge the gap between our understanding of human brains and the brains of other mammals.

Tenascin proteins inhibit cell sheath regeneration

Juliane Bauch (left) and Andreas Faissner from the Chair of Cell Morphology and Molecular Neurobiology
Credit: RUB, Kramer

In multiple sclerosis, nerve cells lose their insulating layer. Researchers from Bochum are looking for starting points to promote regeneration processes. They have identified two relevant proteins.

Researchers at the Ruhr University Bochum have investigated the role that the two proteins tenascin C and tenascin R play in multiple sclerosis. In the disease, cells of the immune system destroy the myelin sheaths, i.e. the sheathing of the nerve cells. As the Bochum team showed in experiments with mice, the presence of the two Tenascins inhibits the regeneration of the myelin sheaths. Dr. Juliane Bauch and Prof. Dr. Andreas Faissner from the Bochum Chair for Cell Morphology and Molecular Neurobiology describes the results in the journal Cells.

The cause of the destruction of myelin sheaths in multiple sclerosis has not yet been clarified. "But the organism has various mechanisms to partially compensate for the lesions," says Juliane Bauch, who dealt intensively with the topic in her doctorate. The aim of the work is to identify starting points with which the regeneration of myelin sheaths could be improved.